Skip to main content


DNA damage protection: an excellent application of bioactive compounds


Discovery of deoxyribonucleic acid (DNA) solved out the mystery of cellular functioning and abnormality in cellular metabolism. Understanding the coding of DNA resulted in enormous medical growth and helps the researchers in finding the genes which trigger major chronic diseases in humans. Further, the structural and sequential analysis brought humans into a new era of medical industry. The advancement in understanding of DNA could be a boon for agricultural sector as it allowed the farmers/breeders to choose better varieties with disease resistant features. In developing nations where the staple foods suffers with micronutrient deficiencies and stress conditions, DNA modifications and repair mechanism could solve out their problems. The role of DNA damaging factors and repair mechanism plays a crucial role in occurrence of certain disorders. Extracts prepared from various natural resources could either stop or slow down the process of DNA damage. This will help to eradicate major disorders related to DNA from human race. Further on the basis of type and dose of natural extracts, it would ease the planning of diets for patients suffering from chronic disorders.


Being a complex macromolecule, deoxyribonucleic acid (DNA) controls the important genetic characteristics of living organism. Genes are important segment/sections of DNA that are indirectly involved in coding of proteins which acts as a basic building for cellular system (Singh and Sharma 2018). The majority of genetic information, defects and diseases rely on types of DNA, their structure and functions performed by them within the human body. The effect of several factors (environmental, synthetic chemicals, UV rays, genetic defects) on DNA modulates its functionality within cells and ultimately results in notable changes in the living organisms (Farag and Alagawany 2018). Damage to DNA and its important segments could occur at endogenous level as well as external factors, thereby posing a threat at cellular level (John 1987; Lu et al. 2015). Continuous exposure of DNA and genome of living organisms to damaging factors could result in variety of genetic defects which might be inherited from one generation to the other (Perez-Coyotl et al. 2017; Han et al. 2017). Understanding the molecular structure and functionality of DNA could help scientists to discover new drugs for the treatment of various chronic diseases. In fact, discovery of important genes that are required to sustain normal metabolism in the cells and their subsequent analysis for therapeutic purposes influenced scientific community (Gagna and Lambert 2006). Artificial methods are being employed to change sequences of DNA to achieve desired results in diseased patients and genetic improvement in agricultural sector. DNA is an important molecule to be studied for the welfare of human race (Liu 2017; Sawitzke et al. 2017). Modifications at genetic level could result in drought as well as salt-tolerant crops with maximal yield. DNA modifications are not restricted up to plants system even it could be used for the improvement of animal breeds also. Researchers all over the world are working on the aspect of relating the changes in DNA with evolutionary development (Hefferon 2018; Ma et al. 2017; Hall 2012; Deichmann 2011). Being a complex molecule, DNA has its presence in every cells of body and will help to sustain growth and repair during various metabolic reactions (Turgeon et al. 2018; Shimizu et al. 2014).

The present review covers types of DNA damage (Fig. 1), its importance for living organisms and role of bioactive compounds in preventing DNA damage. This review may help readers to understand the importance of natural resources and their use as a remedy for various disease treatments.

Fig. 1

Types of DNA damages

Radiations-mediated DNA damage

Radiations are being used in the treatment of various diseases and for the welfare of human beings. However, like other scientific discoveries radiations also have some deteriorating effects of living organism (Little 2003). Scientific reports since long time accepted that exposure of living beings to radiations could result in cellular death, DNA damage and early aging problems (Desouky et al. 2015). Everyday living organisms including humans are exposed to radiations; however, the amount of radiations they may face vary as per location, intensity and timing. Deteriorating effects of radiations are dose dependent and characterized by specific threshold value (Tubiana et al. 2007). However, in response to radiations the body of organisms starts cellular defense mechanism: (1) production of antioxidants, (2) activation of detoxifying enzymes (dismutase and catalase), and (3) elimination of old and dead cells via apoptosis phenomenon. Sustainability in biochemical reactions is controlled by specific molecules and enzymatic pathways. Molecular structures may rely on type of specific bonds varying from cells to cells and types of ongoing processes within cells. Slight alteration in chemical bonds may result in observable changes in the pathways and structural components. Radiations act as powerful factors that can affect the living organisms even at DNA level. Dependency of cellular system on radiation dose could result in major changes in the body of living organisms (Scott 2008; Waldren 2004; Joiner et al. 2001; Shadley 1994; Wolff 1992). The radiations affect the living system in two ways: (1) functional death of cells and (2) reproductive failure of cells. Functional death of cells may lead to abnormality in cellular functions due to internal changes in cells. However, in the reproductive failure case, the cells may perform their daily routine functions but despite their performance they are not able to reproduce. Experimental trials are being carried on animals by researchers/scientists for the verification of radiation effects. However, the degree of damage may vary from organism to organisms depending on the type selected for experimental purpose. Experimental data collected from animal studies greatly vary while estimating the genetic risks in humans. Communication mechanism plays an important role during cellular exposure to radiations (Nikjoo and Khvostunov 2004). Adverse effects of radiations are tissues specific even within the single organism. The type of harmful effects may vary from instant response to delayed response depending on the type of tissues, age of organism, exposure time and immune system of exposed organisms.

Oxidative stress (OS) and hydroxyl-mediated DNA damage

The majority of DNA damage occurs in human beings in response to oxidative stress (OS). Human DNA remains continuously in exposure to free radicals attack. Several factors are responsible for the formation of reactive oxygen species (ROS) and free radicals (FRs). The major factors include: change in life style, restless life, types of dietary elements, fried foods/junk foods and smoking (Kaur et al. 2018a, b; Salar and Purewal 2017; Salar et al. 2017a; Chandrasekara and Shahidi 2012). These factors contribute towards imbalance in the formation of FRs and antioxidants within human body (Dhull et al. 2016). The formation of ROS and FRs is a continuous phenomenon that occurs during normal respiration process. These byproducts are accepted as sole factors for OS-mediated injuries in living organisms (Georgakilas et al. 2010; Xiao et al. 2015; Salar et al. 2017b). The formation of bioactive antioxidants within living organisms in response to ROS and FRs is one of the defense mechanisms. Biomarkers played an important role in the assessment of OS, ROS and FRs. The major biomarkers comprise FRs product and ROS in response to certain specific substrate and factors. Analysis of damage using markers creates a bridge between the occurrence of DNA damage and solution to chronic diseases. As the measurement aspects of markers help to determine the adequate amount of specific nutrients to be supplemented in daily routine diets (Bloomer and Fisher-Wellman 2008). The frequency of cellular DNA damage in humans depends on the type and quantity of bioactive constituent's production in response to FRs. Uncontrolled tumor growth increases in response to higher amount of ROS and FRs. Cellular mechanism in those conditions starts releasing cytokines which help in cell signaling during damage/cellular injury (Mantovani et al. 2008). Damage to DNA could occur in two ways: (1) Exogenous and (2) Endogenous (Kryston et al. 2011). Exogenous DNA damage occurs in response to certain specific environmental factors such as X-rays, cosmic rays, UV radiations and secondary pollutants from chemical oxidations (Parplys et al. 2012; Salar et al. 2016). Endogenous DNA damage occurs in response to intracellular cellular disturbance in signaling and various metabolic pathways required to sustain healthy life style (Cadet et al. 2010; Sedelnikova et al. 2010). Several scientific reports suggest that chronic oxidative stress (COS) conditions are strongly associated with carcinogenesis (Hwang and Bowen 2007). Generation of ROS and OS conditions results in modification of DNA bases which leads to abnormality (mutations, translocations, gene inactivation) at genomic level (Toyokuni 2006).

Hydroxyl radicals are responsible for DNA damage via their contribution in ROS and endogenous oxidation (Cadet et al. 1999). During the normal respiration process, superoxide radicals are formed as a side product and contribute to OS conditions. Exposure of cellular system to chemical agents, free radicals and radiations brings carcinogenesis in them which further result in disruption of important biochemical reactions in living organisms. Metabolism of oxygen with in living organisms generates OH, O2 and H2O2 which reacts with the biological macromolecules such as DNA, lipids and proteins causing modification in biochemical pathways. Scientific reports confirmed the formation of tandem lesions in response to OS conditions (Box et al. 1997; Delatour et al. 1998; Cadet et al. 1999). Hydroxyl-mediated DNA damage starts with modification in purine and pyramidine bases along with strand breaks and cross links at various sites. Experimental works are under process to reveal the changes at the level of deoxyribose and sugar hydrogens of DNA duplex. Various complexes formed during the hydroxyl-induced damage prefer to react with specific deoxyribose hydrogen atom and result in abstraction of deoxyribose hydrogens (Hangeland et al. 1992; Kozarich et al. 1989; Sitlani et al. 1992; Balasubramanian et al. 1998).

Chemicals-mediated DNA damage

Chemical agents act as a powerful mutagen which could damage a significant amount of DNA (Auerbach 1976). All the chemical agents are not able to cause DNA damage with in living organisms. However, they are present in inactivated form and need an impulsive response for their activation. During the combustion of non-renewable as well as renewable resources like coal, gas tobacco and gases, some secondary pollutants may form which cause damage to DNA (Noah et al. 2019; Smit et al. 2019; Aucella et al. 2019; Guilbert et al. 2019). Smoking is solely a man-made DNA damaging exogenous process which is more dangerous and plays an important role during tumor formation and induction of lung cancers (Rojewski et al. 2018; Kaufman et al. 2018; Christensen et al. 2018; Donner et al. 2018). In addition to manmade chemicals, certain microorganisms and plant products are also responsible for DNA damage in organisms. Fungal strains produce certain metabolites under harsher conditions or in response to specific media components which contribute to cause certain cancers in humans. The metabolites termed as aflatoxins, especially AFT-B1 produced by Aspergillus spp., acts as hepatocarcinogen which results in abnormality and cirrhosis in liver (Feng et al. 2017; Manova and Gruszka 2015; Hamid et al. 2013; Asim et al. 2011; Barrett 2005; Verma 2004; Jackson and Groopman 1999). A reactive epoxide may form in response to AFT-B1 which reacts at specific position (N7) of guanine and cause metabolic disfunctioning of liver. Certain plants secretes secondary compounds in response to stress conditions which are also cancer inducing. Among carcinogens (limonen, aristolochia acid, arecolin and reserpin) of plant origin, safrol is an important compound to be studied in detail as it found in pepper, celery, and Sassafras albidum which cause cancer.

Relationship between oxidative stress and diseases

Excess formation of free radicals/oxidative stress results in injury to important biomolecules in living organisms (Zhao, 2005; Kaur et al. 2018a, b; Singh et al. 2018a, b). Free radical/oxidative stress creates damaging conditions via different ways and it includes: oxidation of proteins; non-recoverable damage to plasma membrane; and DNA damage. Oxidative stress harbors normal metabolic reactions of brain and relative tissues. Measurable changes at DNA level lead to occurrence of diseases like Alzheimer disease; Parkinson’s disease, early aging and diabetic conditions (Zhao 2005; Butterfield and Kanski 2001; Smith et al. 1996, 1998; Kaur et al. 2018a, b; Singh et al. 2018a, b).

Scientific reports suggest that there is relationship between onset of diabetic symptoms and oxidative stress. Free radicals/reactive oxygen species have unique capability to bind with lipids, proteins and DNA and there binding results in progression of late diabetic complication (Ayepola et al. 2014). Various in vivo studies carried out by researchers support the role of hyperglycemia in the generation of oxidative stress which further results in endothelial dysfunction in blood vessels of diabetic patients (Ullah et al. 2016; Ceriello 2006). Sharp increase in blood glucose and dyslipidemia in diabetic patients results in formation of macroangiopathies that cause atherosclerosis (Giugliano et al. 1995).

Healthy diet rich in minerals, antioxidants and other important nutrients may slow down the rate of pathogenesis. Micronutrients played an important role in sustaining various metabolic reactions within the body (Li et al. 2014; Dhull et al. 2016). Vitamins B6, B12 and folic acid are reported to play a role in metabolism of homocysteine. Increased level of homocysteine than normal in the plasma of patients with AD has been reported (Dudkowiak et al. 2016; Malaguarnera et al. 2004).

Blockage in major blood circulating pathway leads to sudden stroke and death of major population throughout the world. Change in blood composition and DNA damage is the major leading factor that causes death. The formation of free radicals/reactive oxygen species results in long-term disability in peoples of every age. Oxidative stress could cause disturbance in mitochondrial chain, ischemia-activated xanthine/hypoxanthine oxidase and imbalance in fatty acid metabolism (Taleb et al. 2018; Johnson et al. 2018; Sagoo and Gnudi 2018; Li et al. 2018; Lin et al. 2018). With increase in the activity of free radicals during oxidative destruction and nonreplicating nature of the neuronal cells, the brain is much susceptible to the damage caused (Traystman et al. 1991). Researchers explore the effects of bioactive constituents and their antioxidant properties on preventing the neural disorders, early aging and other chronic disorders.

Oxidative stress and Alzheimer’s disease (AD)

During Alzheimer’s disease, amyloid ß (Aß) and tau proteins play an important role in pathogenesis (Ittner and Götz 2011). Accumulation of Aß in the hippocampal region imparts toxic effects and immune response that lead to cognitive impairment (Anantharaman et al. 2006). The collection of Aß in the brain causes the dysfunction of mitochondria and metabolic disturbances as well as increased formation of the ROS (Sheng et al. 2012). The meta-analysis has shown significantly lower plasma levels of folate and vitamins A, B12, C and E in a group of AD patients as compared to control population (Dudkowiak et al. 2016). There is a strong belief that vitamin A, vitamin C and vitamin E which are antioxidants may be beneficial in slowing the progression and preventing AD (Dudkowiak et al. 2016; Di Domenico et al. 2015; Morris 2009).

Bioactive compounds for DNA damage protection

Diets enriched with natural constituents offer protection against the development of cardiovascular diseases (CVD), diabetes and cancer (Brevik et al. 2011; Jenkins et al. 2003; Ness and Powles 1997). Loss in functionality of macromolecules is a result of accumulation of oxidative stress and ROS which ultimately result in occurrence of diabetes, inflammation, Parkinson’s and Alzheimer’s diseases, and cancer (Salar et al. 2012; Benz and Yau 2008). Decline in mitochondrial efficacy with increasing age would result in release of maximal reactive oxygen which harbors DNA repair mechanism (Gedik et al. 2005; Fraga et al. 1990; Kaneko et al. 1996; Izzotti et al. 1999). Natural resources with antioxidant properties have played a significant role in providing the better health to human race.

Natural resources (fruit, vegetables, cereal grains and medicinal plants) are considered as a rich source of bioactive components (vitamins, antioxidants, anthocyanins, sterols and minerals) (Neri-Numa et al. 2018). Because of natural antioxidants, fruits and vegetable act as a complementary and an alternative medicinal therapeutic modality (Singh et al. 2018a, b; Brevik et al. 2011). Bioactive components possess antiproliferative, antimicrobial, antioxidant, hypoglycemic and DNA damage protection activities (Kaur et al. 2018a, b; Salar and Purewal 2017; Nile and Park 2014). Bitter component (Naringenin) present in citrus fruits has shown promising results in the treatment of metabolic disorders (Alam et al. 2014) and its anti-cancer (Krishnakumar et al. 2011) and chemo-sensitizing properties are also reported (Bao et al. 2016; Abaza et al. 2015; Ahamad et al. 2014). Naringenin inhibited azoxymethane-induced colon carcinogenesis and protected plasmid DNA from UVB-induced DNA damage (Kootstra 1994). Antioxidant-rich natural resources are grown all over the world for their health benefiting secondary metabolites and functional products (Salar et al. 2017a; Dhull et al. 2016; Mikulic-Petkovsed et al. 2012; Szajdek and Borowska 2008). Multifunctional bioactive components present in natural resources are solvent specific (Liyana-Pathirana and Shahidi 2005; Cheok et al. 2012) and sensitive for extraction parameters (extraction phase, temperature and time) (Arruda et al. 2017; Salar et al. 2016). Bioactive components include: phenolic compounds, flavonoids, tannins and other important phytochemicals (saponins, catechol tannin, anthocyanin, steroids and sugars) (Salar et al. 2015; Salar and Purewal 2016; Siroha et al. 2016). Quercetin is an important bioactive constituent with antioxidant properties which has shown many health benefits including cancer prevention and treatment (Chirumbolo 2013; Russo et al. 2012; Bischo 2008). Scientific reports suggest that quercetin can interact with human telomerase sequences and stabilizes the G-quadruplex structure (Tawani and Kumar 2015). DNA duplex may form during the binding of flavonoids with DNA which protect DNA from the oxidative damage (Tiwari and Mishra 2017; Kanakis et al. 2006). Quercetin can affect the rate of formation of ROS, thus reducing the number of lesions in PC12 neuronal cells (Silva et al. 2008). Quercetin has capability enough to arrest cell cycle at specific points resulting in induction of mitochondrial pathway of apoptosis (Srivastava et al. 2016). Factors affecting the recoverable amount of bioactive components from natural resources need optimization. Response surface methodology is one of the important software that are being used by researchers/scientists for optimization purpose (Gilhotra et al. 2018; Singh et al. 2018a, b; Aggarwal et al. 2017; Singh et al. 2017; Bhatia et al. 2016).

Use of natural resources for DNA damage protection activity

Natural resources with potent antioxidants and bioactive constituents should be analyzed in an array of model systems. The efficacy of bioactive constituents depends on soil profile, moisture content, stress conditions and nutrient absorption rate by the natural resources under a given set of conditions. However, suitable analytical protocols need to be adopted to monitor the kinetics of antioxidants during OS conditions. Extracts prepared from specific natural resources are currently being used against Fenton’s reagent for the protection of DNA from oxidative damage (Table 1). Considering the medicinal properties and broad spectrum applications present in natural resources for the welfare of human race, it is most important to identify the regulatory components/mechanisms involved in the whole process. The detailed knowledge of phytoconstituents helps plant breeder to screen out the best cultivars on the basis of specific properties they possess. Moreover, the relationship between the diet, stress conditions and DNA repair is of utmost importance. Stability of genomic DNA is maintained by the plants mainly in three counterparts: (1) chloroplast, (2) mitochondria and (3) nuclei. Several scientific reports suggest that during the evolutionary changes the simplified organelles build up symbiotic relationships with eukaryotic ones. Experimental studies are being carried out on various resources to identify the relationship among organelles, DNA damaging factors and repair systems. Significant DNA damage protection activity in extracts such as [Barley (Salar et al. 2017a); pearl millet (Salar et al. 2017b); Mung beans (Xiao et al. 2015); Grape seeds (Aybastier et al. 2018); Ashtvarga (Giri et al. 2017); Amazon moss (Fernandes et al. 2018); Sugarcane (Abbas et al. 2014); Eulophia nuda Lindl. (Kumar et al. 2013); Honey (Habib et al. 2014); Carissa carandas leaves (Verma et al. 2015); Bael flower (Chandrasekara et al. 2018); Teucrium polium and Stachys iberica (Tepe et al. 2011); Sphallerocarpus gracilis seeds (Gao et al. 2014); Garcinia gracilis leaves (Supasuteekul et al. 2016) was reported. Protocol for the preparation of extracts for DNA damage protection activity is summarized in Fig. 2. DNA damage resulted in breakdown of one of the phosphodiester chains in response to Fenton’s reagent during agarose gel electrophoresis. In response to hydroxyl radicals, the supercoiled form of DNA changes into a relaxed form. Fenton’s reagent-mediated reaction complex leads to the formation of hydroxyl radical in the presence of hydrogen peroxide (H2O2) and Fe3+. Breakdown of DNA strand may cause chronic diseases and age-related medical issues (Guleria et al. 2017; Gao et al. 2014).

Table 1 DNA damage protection activity in extracts prepared from natural resources
Fig. 2

Protocol for the preparation of extracts for DNA damage protection activity


Antioxidants enriched natural resources have efficiency to protect DNA from damaging effects of radiations as well as Fenton’s reagent. Bioactive constituents and their derivative are directly/indirectly involved in slowing down the effect of carcinogenic agents. Effective exercise, natural extracts, balanced diet and daily routine activities which involve less stress could be a remedy for DNA damage protection. Further studies are required to elaborate the deep mechanism involved in DNA repair pathways. Toxicity analysis is necessary before the use of purified compounds in therapeutic purposes.



deoxyribonucleic acid


oxidative stress


reactive oxygen species


free radicals


chronic oxidative stress

H2O2 :

hydrogen peroxide


Alzheimer’s disease


cardiovascular disease


  1. Abaza MS, Orabi KY, Al-Quattan E, Al-Attiyah RJ (2015) Growth inhibitory and chemo-sensitization effects of naringenin, a natural flavanone purified from Hymus vulgaris, on human breast and colorectal cancer. Cancer Cell Int 15:46.

  2. Abbas SR, Sabir SM, Ahmad SD, Boligon AA, Athayde ML (2014) Phenolic profile, antioxidant potential and DNA damage protecting activity of sugarcane (Saccharum officinarum). Food Chem 147:10–16.

  3. Aggarwal L, Sinha S, Bhatti MS, Gupta VK (2017) Mixer design optimization with fractured surface topography of mechanical properties of polymer biocomposites. J Taiwan Inst Chem Eng 74:272–280.

  4. Ahamad MS, Siddiqui S, Jafri A, Ahmad S, Afzal M, Arshad M (2014) Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinoma cell through ROS generation and cell cycle arrest. PLoS ONE 9:e110003.

  5. Alam MA, Subhan N, Rahman MM, Uddin SJ, Reza HM, Sarker SD (2014) Effect of citrus flavonoids, naringin and naringenin, on metabolic syndrome and their mechanisms of action. Adv Nutr 5:404–417.

  6. Anantharaman M, Tangpong J, Keller JN, Murphy MP, Markesbery WR, Kiningham KK, Clair DK (2006) Beta-amyloid mediated nitration of manganese superoxide dismutase: implication for oxidative stress in a APPNLH/NLH X PS-1P264L/P264L double knock-in mouse model of Alzheimer’s disease. Am J Pathol 168:1608–1618.

  7. Arruda HS, Pereira GA, Pastore GM (2017) Optimization of extraction parameters of total phenolics from Annona crassiflora Mart. (Araticum) fruits using response surface methodology. Food Anal Meth 10:100–110.

  8. Asim M, Sarma MP, Thayumanavan L, Kar P (2011) Role of Aflatoxin B1 as a risk for primary liver cancer in north Indian population. Clin Biochem 44:1235–1240.

  9. Aucella F, Prencipe M, Gatta G, Aucella F, Gesualdo L (2019) Environment, smoking, obesity, and the kidney. In: Critical care nephrology (Third Edition). pp 1320–1324.e1

  10. Auerbach C (1976) Chemical mutagens: alkylating agents. II: Chemistry. Molecular analysis of mutants. Influence of cellular processes. Kinetics. In: Mutation research. Springer, Boston

  11. Aybastier O, Dawbaa S, Demir C (2018) Investigation of antioxidant ability of grape seeds extract to prevent oxidatively induced DNA damage by gas chromatography-tandem mass spectrometry. J Chromatogr B 1072:328–335.

  12. Ayepola OR, Brooks NL, Oguntibeju OO (2014) Oxidative stress and diabetic complications: the role of antioxidant vitamins and flavonoids. pp 25–58

  13. Balasubramanian B, Pogozelski WK, Tullius TD (1998) DNA strand breaking by the hydroxyl radical is governed by the accessible surface areas of the hydrogen atoms of the DNA backbone. Proc Natl Acad Sci U S A 95:9738–9743.

  14. Bao L, Liu F, Guo HB, Li Y, Tan BB, Zhang WX, Peng YH (2016) Naringenin inhibits proliferation, migration, and invasion as well as induces apoptosis of gastric cancer SGC7901 cell line by downregulation of AKT pathway. Tumour Biol 37:11365–11374.

  15. Barrett JR (2005) Liver cancer and aflatoxin: new information from the Kenyan outbreak. Environ Health Prosp 113:A837–A838.

  16. Benz CC, Yau C (2008) Ageing, oxidative stress and cancer: paradigms in parallax. Nat Rev Cancer 8:875–879.

  17. Bhatia JK, Kaith BS, Singla R, Mehta P, Yadav V, Dhiman J, Bhatti MS (2016) RSM optimized soy protein fibre as a sorbent material for treatment of water contaminated with petroleum products. Desalin Water Treat 57:4245–4254.

  18. Bischo SC (2008) Quercetin: potentials in the prevention and therapy of disease. Curr Opin Clin Nutr Metab Care 11:733–740.

  19. Bloomer RJ, Fisher-Wellman KH (2008) Blood oxidative stress biomarkers: influence of sex, exercise training status, and dietary intake. Gend Med 5:218–228.

  20. Box HC, Budzinski EE, Dawidzik JB, Gobey JS, Freund HG (1997) Free radical-induced tandem base damage in DNA oligomers. Free Radic Biol Med 23:1021–1030.

  21. Brevik A, Gaivao I, Medin T, Jorgenesen A, Piasek A, Elilasson J, Karlsen A, Blomhoff R, Veggan T, Duttaroy AK, Collins AR (2011) Supplementation of a western diet with golden kiwifruits (Actinidia chinensis var.’Hort 16A’:) effects on biomarkers of oxidation damage and antioxidant protection. Nutr J 10:54.

  22. Butterfield DA, Kanski J (2001) Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins. Mech Ageing Dev 122:945–962

  23. Cadet J, Delatour T, Douki T, Gasparutto D, Pouget JP, Ravanat JL, Sauvaigo S (1999) Hydroxyl radicals and DNA base damage. Mut Res 424:9–21.

  24. Cadet J, Douki T, Ravanat JL (2010) Oxidatively generated base damage to cellular DNA. Free Radic Biol Med 49:9–21.

  25. Ceriello A (2006) Oxidative stress and diabetes-associated complications. Endocr Pract 12:60–62.

  26. Chandrasekara A, Shahidi F (2012) Bioaccessibility and antioxidant potential of millet grain phenolics as affected by simulated in vitro digestion and microbial fermentation. J Funct Foods 4:226–237.

  27. Chandrasekara A, Daugelaite J, Shahidi F (2018) DNA scission and LDL cholesterol oxidation inhibition and antioxidant activities of Bael (Aegle marmelos) flower extracts. J Tradit Complement Med 8:428–435.

  28. Cheok CY, Chin NL, Yusof AY, Talib RA, Law CL (2012) Optimization of total phenolic content extracted from Garcinia mangostana Linn. Hull using response surface methodology versus artificial neural network. Indus Crop Prod 40:247–253.

  29. Chirumbolo S (2013) Quercetin in cancer prevention and therapy. Integr Cancer Her 12:97–102.

  30. Christensen NL, Lokke A, Dalton SO, Christensen J, Rasmussen TR (2018) Smoking, alcohol, and nutritional status in relation to one-year mortality in Danish stage I lung cancer patients. Lung Cancer 124:40–44.

  31. Deichmann U (2011) Early 20th-century research at the interfaces of genetics, development, and evolution: reflections on progress and dead ends. Dev Biol 357:3–12.

  32. Delatour T, Douki T, Gasparutto D, Brochier MC, Cadet J (1998) A novel vicinal lesion obtained from the oxidative photosensitization of TpdG: characterization and mechanistic aspects. Chem Res Toxicol 11:1005–1013.

  33. Desouky O, Ding N, Zhou G (2015) Targeted and non-targeted effects of ionizing radiation. J Radiat Res Appl Sci 8:247–254.

  34. Dhull SB, Kaur P, Purewal SS (2016) Phytochemical analysis, phenolic compounds, condensed tannin content and antioxidant potential in Marwa (Origanum majorana) seed extracts. Resour Efficient Technol 2:168–174.

  35. Di-Domenico F, Barone E, Perluigi M, Butterfield DA (2015) Strategy to reduce free radical species in Alzheimer’s disease: an update of selected antioxidants. Expert Rev Neurother 15:19–40.

  36. Donner L, Katainen R, Sipila LJ, Aavikko M, Pukkala E, Aaltonen LA (2018) Germline mutations in young non-smoking women with lung adenocarcinoma. Lung Cancer 122:76–82.

  37. Dudkowiak R, Gryglas A, Poniewierka E (2016) The role of diet and antioxidants in the prevention of Alzheimer’s disease. J Med Sci 85:205–212.

  38. Farag MR, Alagawany M (2018) Erythrocytes as a biological model for screening of xenobiotics toxicity. Chem Biol Interact 279:73–83.

  39. Feng WH, Xue KS, Tang L, Williams PL, Wang JS (2017) Aflatoxin B1-induced developmental and DNA damage in caenorhabditis elegans. Toxins (Basel) 9:1–12.

  40. Fernandes AS, Mazzei JL, Evangelista H, Marques MRC, Ferraz ERA, Felzenszwalb I (2018) Protection against UV-induced oxidative stress and DNA damage by Amazon moss extracts. J Photochem Photobiol B 183:331–341.

  41. Fraga C, Shigenaga MK, Park J, Degan P, Ames BN (1990) Oxidative damage to DNA during aging; 8-hydroxy-2′-deoxyguanosine in rat organ DNA and urine. Proc Nat Acad Sci U S A 87:4533–4537

  42. Gagna CE, Lambert WC (2006) Novel drug discovery and molecular biological methods, via DNA, RNA and protein changes using structure–function transitions: transitional structural chemogenomics, transitional structural chemoproteomics and novel multi-stranded nucleic acid microarray. Med Hypotheses 67:1099–1114.

  43. Gao CY, Tian C, Zhou R, Zhang R, Lu Y (2014) Phenolic composition, DNA damage protective activity and hepatoprotective effect of free phenolic extract from Sphallerocarpus gracilis seeds. Int Immunopharmacol 20:238–247.

  44. Gedik CM, Grant G, Morrice PC, Wood SG, Collins AR (2005) Effects of age and dietary restriction on oxidative DNA damage, antioxidant protection and DNA repair in rats. Eur J Nutr 44:263–272.

  45. Georgakilas AG, Mosley W, Georgakila S, Zeich D, Panayiotidis MI (2010) Viral-induced human carcinogenesis: an oxidative stress perspective. Mol BioSyst 6:1162–1172.

  46. Gilhotra V, Das L, Sharma A, Kang TS, Singh P, Dhuria RS, Bhatti MS (2018) Electrocoagulation technology for high strength arsenic wastewater: process optimization and mechanistic study. J Clean Prod 198:693–703.

  47. Giri L, Belwal T, Bahukhandi A, Suyal R, Bhatt ID, Rawal RS, Nandi SK (2017) Oxidative DNA damage protective activity and antioxidant potential of Ashtvarga species growing in the Indian Himalayan Region. Ind Crop Prod 102:173–179.

  48. Giugliano D, Ceriello A, Paolisso G (1995) Diabetes mellitus, hypertension, and cardiovascular disease: which role for oxidative stress? Metabolism 44:363–368

  49. Guilbert A, Cremer KD, Heene B, Demoury C, Aerts R, Declerck P, Brasseur O, Nieuwenhuyse AV (2019) Personal exposure to traffic-related air pollutants and relationships with respiratory symptoms and oxidative stress: a pilot cross-sectional study among urban green space workers. Sci Tot Env 649:620–628.

  50. Guleria S, Singh G, Gupta S, Vyas D (2017) Antioxidant and oxidative DNA damage protective properties of leaf, bark and fruit extracts of Terminalia chebula. Indian J Biochem Biophy 54:127–134.

  51. Habib HM, Al-Meqbali FT, Kamal H, Souka UD, Ibrahim WH (2014) Bioactive components, antioxidant and DNA damage inhibitory activities of honeys from arid regions. Food Chem 153:28–34.

  52. Hall BK (2012) Evolutionary developmental biology (Evo-Devo): past, present, and future. Evol Edu Outreach 5:184–193.

  53. Hamid AS, Tesfamariam IG, Zhang Y, Zhang ZG (2013) Aflatoxin B1-induced hepatocellular carcinoma in developing countries: geographical distribution, mechanism of action and prevention. Oncol Lett 5:1087–1092.

  54. Han JH, Lee HJ, Choi HJ, Yun KE, Kang MH (2017) Lymphocyte DNA damage and plasma antioxidant status in Korean subclinical hypertensive patients by glutathione S-transferase polymorphism. Nutr Res Pract 11:214–222.

  55. Hangeland JJ, De Voss JJ, Heath JA, Townsend CA, Ding WD, Ashcroft J, Ellestad GA (1992) Specific abstraction of the 5′S- and 4′-deoxyribosyl hydrogen atoms from DNA by calicheamicin.gamma.1I. J Am Chem Soc 114:9200–9202.

  56. Hasnat MA, Pervin M, Kim DH, Kim YJ, Lee JJ, Pyo HJ, Lee CW, Lim BO (2015) DNA protection and antioxidant and anti-inflammatory activities of water extract and fermented hydrolysate of Abalone (Haliotis discus hannai Ino). Food Sci Biotechnol 24:689–697.

  57. Hefferon KL (2018) Chapter 16—crops with improved nutritional content though agricultural biotechnology. Plant Micronutrient Use Efficiency, 279–294

  58. Hwang ES, Bowen PE (2007) DNA damage, a biomarker of carcinogenesis: its measurement and modulation by diet and environment. Crit Rev Food Sci Nutr 47:27–50.

  59. Ittner LM, Götz J (2011) Amyloid-β and tau—a toxic pas de deux in Alzheimer’s disease. Nat Rev Neurosci 12:65–72.

  60. Izzotti A, Cartiglia C, Taningher M, De Flora S, Balansky R (1999) Age-related increases of 8-hydroxy-2′-deoxyguanosine and DNA-protein crosslinks in mouse organs. Mutat Res 446:215–223

  61. Jackson PE, Groopman JD (1999) Aflatoxin and liver cancer. Best Prac Res Clin Gastroenterol 13:545–555

  62. Jenkins DJ, Kendall CW, Marchie A, Jenkins AL, Augustin LS, Ludwig DS, Barnard ND, Anderson JW (2003) Type 2 diabetes and the vegetarian diet. Am J Clin Nutr 78:610S–616S.

  63. John WC (1987) The metabolism of xenobiotic chemicals. J Chem Educ 64:396.

  64. Johnson P, Loganathan C, Iruthayaraj A, Poomani K, Thayumanavan P (2018) S-allyl cysteine as potent anti-gout drug: insight into the xanthine oxidase inhibition and anti-inflammatory activity. Biochimie 154:1–9.

  65. Joiner MC, Marples B, Philippe-Lambin MD, Susan C, Ingela-Turesson MD (2001) Low-dose hypersensitivity: current status and possible mechanisms. Int J Radiat Oncol Biol Phys 49:379–389.

  66. Kanakis CD, Tarantilis PA, Polissiou MG, Tajmir-Riahi HA (2006) Interaction of antioxidant flavonoids with tRNA: intercalation or external binding and comparison with flavonoid-D1A adducts. DNA Cell Biol 25:116–123.

  67. Kaneko T, Tahara S, Matsuo M (1996) Non-linear accumulation of 8-hydroxy-2′-deoxyguanosine, a marker of oxidized DNA damage, during aging. Mutat Res 316:277–285.

  68. Kaufman AR, Dwyer LA, Land SR, Klein WMP, Park ER (2018) Smoking-related health beliefs and smoking behavior in the National Lung Screening Trial. Addict Behav 84:27–32.

  69. Kaur P, Dhull SB, Sandhu KS, Salar RK, Purewal SS (2018a) Tulsi (Ocimum tenuiflorum) seeds: in vitro DNA damage protection, bioactive compounds and antioxidant potential. Food Meas 12:1530–1538.

  70. Kaur R, Kaur M, Purewal SS (2018b) Effect of incorporation of flaxseed to wheat rusks: Antioxidant, nutritional, sensory characteristics, and in vitro DNA damage protection activity. J Food Process Preserv.

  71. Khurana R, Karan R, Kumar A, Khare SK (2010) Antioxidant and antimicrobial activity in some Indian herbal plants: protective effect against free radical mediated DNA Damage. J Plant Biochem Biotechnol 19:229–233.

  72. Kootstra A (1994) Protection from UV-B-induced DNA damage by flavonoids. Plant Mol Biol 26:771–774.

  73. Kozarich JW, Worth L Jr, Frank BL, Christner DF, Vanderwall DE, Stubbe J (1989) Sequence specific isotope effects on the cleavage of DNA by bleomycin. Science 245:1396–1399

  74. Krishnakumar N, Sulfikkarali N, RajendraPrasad N, Karthikeyan S (2011) Enhanced anticancer activity of naringenin-loaded nanoparticles in human cervical (HeLa) cancer cells. Biomed Prevent Nutr 1:223–231.

  75. Kryston TB, Georgiev AB, Pissis P, Georgakilas AG (2011) Role of oxidative stress and DNA damage in human carcinogenesis. Mut Res 711:193–201.

  76. Kumar A, Lemos M, Sharma M, Shriram M (2013) Antioxidant and DNA damage protecting activities of Eulophia nuda Lindl. Free Radic Antiox 3:55–60.

  77. Li S, Chen G, Zhang C, Wu M, Wu S, Liu Q (2014) Research progress of natural antioxidants in foods for the treatment of diseases. Food Sci Human Wellness 3:110–116.

  78. Li LZ, Zhou GX, Li J, Jiang W, Liu BN, Zhou W (2018) Compounds containing trace element copper or zinc exhibit as potent hyperuricemia inhibitors via xanthine oxidase inactivation. J Trace Elem Med Biol 49:72–78.

  79. Limmongkon A, Pankam J, Somboon T, Wongshaya P, Nopprang P (2018) Evaluation of the DNA damage protective activity of the germinated peanut (Arachis hypogaea) in relation to antioxidant and anti-inflammatory activity. LWT Food Sci Technol 101:259–268.

  80. Lin KH, Yang YY, Yang CM, Huang MY, Lo HF, Liu KC, Lin HS, Chao PY (2013) Antioxidant activity of herbaceous plant extracts protect against hydrogen peroxide-induced DNA damage in human lymphocytes. BMC Res Notes 6:490.

  81. Lin HY, Chang TC, Chang ST (2018) A review of antioxidant and pharmacological properties of phenolic compounds in Acacia confuse. J Tradit Complement Med 8:443–450.

  82. Little MP (2003) Risks associated with ionizing radiation. Br Med Bull 68:259–275

  83. Liu S (2017) Chapter-13 evolution and genetic engineering. bioprocess engineering (Second Edition), pp 783–828.

  84. Liyana-Pathirana C, Shahidi F (2005) Optimization of extraction of phenolic compounds from wheat using response surface methodology. Food Chem 93:47–56.

  85. Lu K, Mahbub R, Fox JG (2015) Xenobiotics: interaction with the intestinal microflora. ILAR J 56:218–227.

  86. Ma Q, Zhang W, Xiang QY (2017) Evolution and developmental genetics of floral display—a review of progress. J Syst Evol 55:487–515.

  87. Malaguarnera M, Ferri R, Bella R (2004) Homocysteine, vitamin B12 and folate in vascular dementia and in Alzheimer disease. Clin Chem Lab Med 42:1032–1035.

  88. Manova V, Gruszka D (2015) DNA damage and repair in plants-from models to crops. Front Plant Sci 6:885.

  89. Mantovani A, Allavena P, Sica A, Balkwill F (2008) Cancer-related inflammation. Nature 454:436–444.

  90. Mikulic-Petkovsed M, Schmitzer V, Slantar A, Stampar F, Veberic R (2012) Composition of sugars, organic acids, and total phenolics in 25 wild or cultivated berry species. J Food Sci 77:1064–1070.

  91. Morris MC (2009) The role of nutrition in Alzheimer’s disease: epidemiological evidence. Eur J Neurol 16:1–7.

  92. Neri-Numa IA, Sancho RAS, Pereira APA, Pastore GM (2018) Small Brazilian wild fruits: nutrients, bioactive compounds, health-promotion properties and commercial interest. Food Res Int 103:345–360.

  93. Ness AR, Powles JW (1997) Fruit and vegetables, and cardiovascular disease: a review. Int J Epidemiol 26:1–13

  94. Nikjoo H, Khvostunov IK (2004) A theoretical approach to the role and critical issues associated with bystander effect in risk estimation. Human Exp Toxicol 23:81–86.

  95. Nile SH, Park W (2014) Edible berries: bioactive components and their effect on human health. Nutr 30:134–144.

  96. Noah S, Rozich MD, Alessandra LMD, Casey S, Butler MD, Morgan M, Bonds MD, Laura E, Fischer MD, Russell G, Postier MD, Katherine T, Morris MD (2019) Tobacco smoking associated with increased anastomotic disruption following pancreaticoduodenectomy. J Surg Res 233:199–206.

  97. Park JH, Seo BY, Lee SC, Park E (2010) Effects of ethanol extracts from stalked sea squirt (Styela clava) on antioxidant potential, oxidative DNA Damage and DNA Repair. Food Sci Biotechnol 19:1035–1040.

  98. Parplys AC, Petermann E, Petersen C, Dikomey E, Borgmann K (2012) DNA damage by X-rays and their impact on replication processes. Radiother Oncol 102:466–471.

  99. Perez-Coyotl I, Martinez-Vieyra C, Galar-Martinez M, Gomez-Olivan LM, Garcia-Medina S (2017) DNA damage and cytotoxicity induced on common carp by pollutants in water from an urban reservoir. Madin reservoir, a case study. Chemosphere 185:789–797.

  100. Rachitha P, Krupashree K, Jayashree GV, Kandikattu HK, Amruta N, Gopalan N, Rao MK, Khanum F (2018) Chemical composition, antioxidant potential, macromolecule damage and neuroprotective activity of Convolvulus pluricaulis. J Tredit Complement Med 8:483–496.

  101. Rojewski AM, Tanner MD, Dai L, Ravenel MD, Mulugeta G, Silvestri GA, Toll BA (2018) Tobacco dependence predicts higher lung cancer and mortality rates and lower rates of smoking cessation in the National Lung Screening Trial. Chest 154:110–118.

  102. Russo M, Spagnuolo C, Tedesco I, Bilotto S, Russo GL (2012) The flavonoid quercetin in disease prevention and therapy: facts and fancies. Biochem Pharmacol 83:6–15.

  103. Sagoo MK, Gnudi L (2018) Diabetic nephropathy: is there a role for oxidative stress? Free Radic Biol Med 116:50–63.

  104. Salar RK, Purewal SS (2016) Improvement of DNA damage protection and antioxidant activity of biotransformed pearl millet (Pennisetum glaucum) cultivar PUSA-415 using Aspergillus oryzae MTCC 3107. Biocatal Agric Biotechnol 8:221–227.

  105. Salar RK, Purewal SS (2017) Phenolic content, antioxidant potential and DNA damage protection of pearl millet (Pennisetum glaucum) cultivars of North Indian region. Food Meas 11:126–133.

  106. Salar RK, Certik M, Brezova V (2012) Modulation of phenolic content and antioxidant activity of maize by solid state fermentation with Thamnidium elegans CCF 1456. Biotechnol Bioprocess Eng 17:109–116.

  107. Salar RK, Sharma P, Purewal SS (2015) In vitro antioxidant and free radical scavenging activities of stem extract of Euphorbia trigona Miller. Tang [Humanitas Medicine] 5:1–6.

  108. Salar RK, Purewal SS, Bhatti MS (2016) Optimization of extraction condition and enhancement of phenolic content and antioxidant activity of pearl millet fermented with Aspergillus awamori MTCC-548. Resour Efficient Technol 2:148–157.

  109. Salar RK, Purewal SS, Sandhu KS (2017a) Relationships between DNA damage protection activity, total phenolic content, condensed tannin content and antioxidant potential among Indian barley cultivars. Biocatal Agric Biotechnol 11:201–206.

  110. Salar RK, Purewal SS, Sandhu KS (2017b) Fermented pearl millet (Pennisetum glaucum) with in vitro DNA damage protection activity, bioactive compounds and antioxidant potential. Food Res Int 100:204–210.

  111. Sawitzke JA, Thomason LC, Costantino N, Court DL (2017) Recombineering: a modern approach to genetic engineering. Ref Module Life Sci 2013:109–112.

  112. Scott BR (2008) It’s time for a new low-dose-radiation risk assessment paradigm-one that acknowledges hormesis. Dose Response 6:333–351.

  113. Sedelnikova OA, Redon CE, Dickey JS, Nakamura AJ, Georgakilas AG, Bonner WM (2010) Role of oxidatively induced DNA lesions in human pathogenesis. Mut Res 704:152–159.

  114. Shadley JD (1994) Chromosomal adaptive response in human lymphocytes. Radiat Res 138:S9–S12

  115. Sheng B, Wang X, Su B, Lee HG, Casadesus G, Perry G, Zhu X (2012) Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer’s disease. J Neurochem 120:419–429.

  116. Shimizu L, Yoshida Y, Suda M, Minamino T (2014) DNA damage response and metabolic disease. Cell Metabol 20:967–977.

  117. Silva JP, Gomes AC, Coutinho OP (2008) Oxidative DNA damage protection and repair by polyphenolic compounds in PC12 cells. Eur J Pharmacol 601:50–60.

  118. Singh N, Sharma B (2018) Biotoxins mediated DNA damage and role of phytochemicals in DNA protection. Biochem Mol Bio J 4:5

  119. Singh H, Bhatti MS, Reddy AS (2017) Decolourization of textile dyebath chloride rich wastewater by electrolytic processes. Int J Electrochem Sci 12:3662–3674

  120. Singh S, Kaur M, Sogi DS, Purewal SS (2018a) A comparative study of phytochemicals, antioxidant potential and in vitro DNA damage protection activity of different oat (Avena sativa) cultivars from India. Food Meas.

  121. Singh S, Sharma S, Umar A, Mehta SK, Bhatti MS, Kansal SK (2018b) Recycling of waste poly (ethylene terephthalate) bottles by alkaline hydrolysis and recovery of pure nanospindle-shaped terephthalic acid. J Nanosci Nanotechnol 18:5804–5809.

  122. Siroha AK, Sandhu KS, Kaur M (2016) Physicochemical, functional and antioxidant properties of flour from pearl millet varieties grown in India. Food Meas 10:1–8.

  123. Sitlani A, Long EC, Pyle AM, Barton JK (1992) DNA photocleavage by phenanthrenequinone diimine complexes of rhodium(III): shape-selective recognition and reaction. J Am Chem Soc 114:2303–2312.

  124. Smit T, Peraza N, Garey L, Langdon KJ, Ditre JW, Rogers AH, Manning K, Zvolensky MJ (2019) Pain-related anxiety and smoking processes: the explanatory role of dysphoria. Addict Behav 88:15–22.

  125. Smith MA, Perry G, Richey PL, Sayre LM, Anderson VE, Beal MF, Kowall N (1996) Oxidative damage in Alzheimer’s disease. Nature 382:120–121

  126. Smith MA, Hirai K, Hsiao K, Pappollo MA, Harris PL, Siedlak SL, Tabaton M, Perry G (1998) Amyloid-beta deposition in Alzheimer transgenic mice is associated with oxidative stress. J Neurochem 70:2212–2215

  127. Srivastava S, Somasagara RR, Hegde M, Nishana M, Tadi SK, Srivastava M, Choudhary B, Raghavan SC (2016) Quercetin, a natural flavonoid interacts with DNA, arrests cell cycle and causes tumor regression by activating mitochondrial pathway of apoptosis. Sci Rep 6:24049

  128. Sudha ML, Dharmesh SM, Pynam H, Bhimangouder SV, Eipson SW, Somasundaram R, Nanjarajurs SM (2016) Antioxidant and cyto/DNA protective properties of apple pomace enriched bakery products. J Food Sci Technol 53:1909–1918.

  129. Supasuteekul C, Nonthitipong W, Tadtong S, Likhitwitayawuid K, Tengamnuay P, Sritularak B (2016) Antioxidant, DNA damage protective, neuroprotective, and -glucosidase inhibitory activities of a flavonoid glycoside from leaves of Garcinia gracilis. Brazilian J Pharmacog 26:312–320

  130. Szajdek A, Borowska EJ (2008) Bioactive compounds and health-promoting properties of berry fruits: a review. Plant Foods Human Nutr 63:147–156.

  131. Taleb A, Ahmad KA, Ullah-Ihsan A, Qu J, Lin N, Hezam K, Koju N, Hui L, Qilong D (2018) Antioxidant effects and mechanism of silymarin in oxidative stress induced cardiovascular diseases. Biomed Pharmacother 102:689–698.

  132. Tang ELH, Rajarajeswaran J, Fung SY, Kanthimathi MS (2013) Antioxidant activity of Coriandrum sativum and protection against DNA damage and cancer cell migration. BMC Complement Altern Med 13:347.

  133. Tawani A, Kumar A (2015) Structural Insight into the interaction of Flavonoids with human telomeric sequence. Sci Rep 5:17574

  134. Tepe B, Degerli S, Arslan S, Malatyali E, Sarikurkcu C (2011) Determination of chemical profile, antioxidant, DNA damage protection and antiamoebic activities of Teucrium poliumand Stachys iberica. Fitoterapia 82:237–246.

  135. Tiwari P, Mishra (2017) Role of flavonoids in DNA damage and carcinogenesis prevention. J Carcinog Mutagen 8:4.

  136. Toyokuni S (2006) Novel aspects of oxidative stress-associated carcinogenesis. Antioxid Redox Signal 8:1373–1377.

  137. Traystman R, Kirsch JR, Koehler C (1991) Oxygen radicals mechanism of brain injury following ischemia and reperfusion. J Appl Phys 71:1185–1195.

  138. Tubiana M, Arengo A, Averbeck D, Masse R (2007) Low-dose risk assessment. Radiat Res 167:742–744

  139. Turgeon M, Perry NJS, Poulogiannis G (2018) DNA damage, repair, and cancer metabolism. Front Oncol 8:15.

  140. Ullah A, Khan A, Khan I (2016) Diabetes mellitus and oxidative stress—a concise review. Saudi Pharm J 24:547–553.

  141. Verma RJ (2004) Aflatoxin cause DNA damage. Int J Human Genet 4:231–236.

  142. Verma K, Shrivastava D, Kumar G (2015) Antioxidant activity and DNA damage inhibition in vitro by a methanolic extract of Carissa carandas (Apocynaceae) leaves. J Taibah Univ Sci 9:34–40.

  143. Waldren CA (2004) Classical radiation biology dogma, bystander effects and paradigm shift. Human Exp Toxicol 23:95–100.

  144. Wolff S (1992) Failla memorial lecture. Is radiation all bad? The search for adaptation. Radiat Res 131:117–123

  145. Xiao Y, Zhang Q, Miao J, Rui X, Li T, Dong M (2015) Antioxidant activity and DNA damage protection of mung beans processed by solid state fermentation with Cordyceps militaris SN-18. Innov Food Sci Emerg Technol 31:216–225.

  146. Zhao B (2005) Natural antioxidants for neurodegenerative diseases. Mol Neurobiol 31:283–293.

Download references

Authors’ contributions

The authors (PK, SSP, KSS and MK) prepared the framework, proofread, corrected and approved the manuscript. All authors read and approved the final manuscript.


The support provided by Department of Food Science & Technology and Department of Biotechnology, Chaudhary Devi Lal University, Sirsa, India is gratefully acknowledged.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

All authors read and approved the manuscript for publication.

Ethics approval and consent to participate

Not applicable.


There is no funding source.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Author information

Correspondence to Sukhvinder Singh Purewal.

Rights and permissions

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Kaur, P., Purewal, S.S., Sandhu, K.S. et al. DNA damage protection: an excellent application of bioactive compounds. Bioresour. Bioprocess. 6, 2 (2019).

Download citation


  • DNA
  • Agriculture
  • Chronic disorders
  • Natural extracts
  • Breeders