Intracellular calcium accumulation had been reported in the liver, kidney, testis, adipose tissue, heart and skeletal muscle of rabbits. Increased accumulation of calcium causes mitochondrial swelling and reduced mitochondrial activity and ATP content thus impairing the operation of the sodium pump.It causes ultrastructural changes in mitochondria and also induces mitochondrial directed apoptosis have also sugges ted thatca lc ium activa ted ca tabolic processes are involved in cytotoxicity.They also indicated that both the enhanced cellular concentration of calcium and the Targetmol’s Gynostemma Extract presence of prooxidant OA uncoupled oxidative phosphorylation resulting increased producing O and hence HO.Possibly an increase in AFB, epoxide cause significantincreasesinhep aticlipidperoxidelevel. Peroxidation of membranelip ids init ia ted loss of membrane in tegrity; membrane bound enzyme activity and cell lysis. The increased lipid peroxidation in aflatoxin treated animals is in agreement with findings reported previously for rat liver. Lipid peroxidation was significantly increased in the liver, kidney of aflatoxintreated mice as compared to controls.The oxidative damage in a cell or tissue occurs species generated exceeds when the concen tration of reactive oxygen the antioxidant capability of the cell. Therefore, it could be due to significant decreases in the levels of nonenzymatic antioxidant and enzymatic antioxidants, which are the maindete rmin antsofthe antioxidantdefencemechanism of the cell.The decline in these enzyme activities could be due to a reduction in protein biosynthesis.Glutathione levels declined significantly in the liver, kidney and testis after days of aflatoxin treatment, which suggests its rapid oxidation.GSH can inhibit peroxidation, scavenge free radicals and pro tectcell membranes. Thus significantly lower GSH levels would further aggravate the toxic effects of aflatoxin.Glutathione has a beneficial effect by virtue of possessing SH groups that help to protectbiologic alm embr anes,whicharere adily susceptible to injury by peroxidation.Breimer reported that free radicals produced in biological membranes rapidly react with alpha tocopheryl radicals.Cytosolic GSH and ascorbic acid help in the regeneration of alpha tocopherol.In addition, oxidative stress may result in damage to crit icalcellu lar macromo lecu les including DNA, lipids and proteins. Cellular fatty acids are readily oxidized by ROS to produce lipid peroxyl radicals which can R.A time and dosedependentincreasein hydroxydeoxy guanosine was observed in rat hepatic DNA after a single intraperitoneal injection of AFB.It indicates that AFB causes oxidative DNA damage in ratl iver thatmay invo lve hydroxyl radicals as the initiation species. Proteins is also easily attacked by ROS directly or indirectly through lipid peroxidation modify their enzyme activity. There is considerable in vitro and in vivo ev idence to support theview thathumanspossess the biochemical processes necessary for aflatoxininduced carcinogenesis.In addition, studies have suggested that oncogenes are critical molecular targets for aflatoxin B.A high frequency of mutations at a mutational hotspot has been found in p tumoursupp ressorgenes in hepa tocellu larcarcinomas from the patients residing in areas considered to offer a high risk of exposure to aflatoxins, and where there is a high incidence of hepatocellular carcinoma. Vitamin E prevents aflatoxininduced lipid peroxidation in liver and kidney.Ameliorative effect of vitamin E on afla tox in inducedlip id pe rox idation in the tes tis of mice.Verma RJ, Raval PJ. Bull Environ Contam Toxicol. Intracellular calcium accumulation during aflatoxicosis.Biochem Pharmacol.