title: Studies on modulation of DNA integrity in Fenton's system by phytochemicals.
abstract: Chronic exposure to oxidative stress especially to highly reactive hydroxyl radicals (HO*) could damage biomolecules, particularly DNA, that in turn would accelerate onset of degenerative diseases. In the present study a few standard phytochemicals (vitamin C, gallic acid, catechin, apigenin, naringenin and naringin) and plant extracts (Hippophae rhamnoides kernel (HRK), Syzygium cumini kernel (SCK) and Punica granatum pericarp (PGP)) were evaluated for their potential to protect/damage DNA in Fenton's system using in vitro models. The results indicated a significant DNA protective effect for naringin and PGP whereas other phytochemicals/extracts showed DNA damaging effect similar to or more than that of control value. The phytochemicals/extracts were also evaluated for their antioxidant and iron chelation properties. In general, the phytochemicals/extracts with high antioxidant activity but without iron chelation capacity failed to protect DNA in Fenton's system, suggesting that iron chelation was an essential requirement for the phytochemicals studied here to retard HO* generation by Fenton's reaction. This was demonstrated by the high iron chelation capacity of naringin and PGP (83.67% and 68.67% respectively) and their DNA protective effect. Commonly consumed phytochemicals such as vitamin C and gallic acid with their high reducing power and at higher physiological concentration, could regenerate free iron for Fenton's reaction leading to DNA damage as shown here.
authors.affiliation: Agro-Processing and Natural Products Division, National Institute for Interdisciplinary Science and Technology, CSIR, Thiruvananthapuram 695019, India. benherlal@gmail.com
authors.forename: Palayyan Saraswathy
authors.initials: PS
authors.lastname: Benherlal
authors.forename: Chami
authors.initials: C
authors.lastname: Arumughan
mesh_terms: D000975:Antioxidants / Q000494:pharmacology; D047310:Apigenin / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D010582:Bacteriophage lambda / Q000187:drug effects / Q000235:genetics; D002392:Catechin / Q000494:pharmacology; D019610:Cytoprotection / Q000187:drug effects; D004249:DNA Damage / Q000502:physiology; D053938:DNA Fragmentation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D044950:Flavanones / Q000494:pharmacology; D005707:Gallic Acid / Q000494:pharmacology; D042822:Genomic Instability / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000493:pharmacokinetics / Q000633:toxicity*; D066298:In Vitro Techniques; D007501:Iron / Q000494:pharmacology / Q000633:toxicity*; D008954:Models, Biological; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; C045076:Fenton's reagent; D044950:Flavanones; D010936:Plant Extracts; D005707:Gallic Acid; D047310:Apigenin; D002392:Catechin; D006861:Hydrogen Peroxide; D007501:Iron; C005273:naringenin; C005274:naringin; D001205:Ascorbic Acid