Visualizing loss of heterozygosity in living mouse cells and tissues

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.