Protective effect of ascorbic acid against oxidative stress induced by inorganic arsenic in liver and kidney of rat.

Ascorbic acid treatment in arsenic trioxide treated rats increased arsenic excretion, inhibited lipid peroxidation, improved GSH status, regulated GSSG turnover and also restored glutathione-S-transferases activity in liver and kidney. Suitable mechanisms leading to ascorbic acid protection have been discussed. Upregulation of GSH dependent enzymes was found to be necessary for a protective effect. Protection is finally attributed to higher GSH levels observed in the liver and kidney of ascorbic acid and inorganic arsenic treated rats. It is also concluded that ascorbic acid protection is influenced by gender dependent factors. Arsenic poisoning is a global problem now. Gender differences need to be considered while applying therapeutic measures.

Modulation of arsenic induced cytotoxicity by tea.

Arsenic, a naturally ocurring chemical element, is considered hazardous to human health. Inorganic arsenic compounds were found to induce cytotoxicity in Chinese hamster V-79 cells in culture. The arsenite form was more toxic than arsenate. Extracts of green and two varieties of black tea, as well as their principal polyphenols, (-)-epigallocatechingallate and theaflavin, efficiently counteracted the cytotoxic effects of arsenic compounds. On the basis of the amount of tea extract that afforded 50% protection to the cells from arsenic induced cytotoxicity, black tea was found to be as effective as green tea. The protective effect was attributable to the contents of not only (-)-epigallocatechingallate but also of theaflavin, the latter being a predominant polyphenol present in black tea.

Central hyperthermic effect of arsenic in rabbits.

Hyperthermic effect of arsenic was investigated in rabbits. Injections of arsenic trioxide (0.0001 to 0.1 micrograms) into a lateral cerebral ventricle of the rabbit evoked a dose-dependent hyperthermia, respiratory stimulation and peripheral vasodilatation. Heat loss through respiratory stimulation and peripheral vasodilatation appeared responsible for the long latent period and the slight hypothermia sometimes obtained during this period as these effects followed the same time course. These effects were centrally mediated as demonstrated by the lack of efficacy of the same doses by the intravenous route. The hyperthermic effect of arsenic was antagonized by the sulphydryl donator, dimercaprol, the a-adrenoceptor blocking agent-phenoxybenzamine and the PG-synthesis inhibitor-aspirin. Multiple sites, for antagonistic effects of these substances can be explained by the action of arsenic in inactivating sulphydryl containing enzymes which are many and catalyze diverse biochemical reactions.