Apoptosis and necrosis in developing brain cells due to arsenic toxicity and protection with antioxidants.

Epidemiological studies on arsenic contamination in drinking water indicated presence of arsenic in fetal tissues. Experiments on human fetal brain explants on exposure to arsenic in culture showed disturbance in lipid peroxidation, generation of nitric oxide (NO), reactive oxygen species (ROS) and apoptosis. The oxidative stress challenged by antioxidant vitamins C, E or chelator dimercaptosuccinic acid (DMSA) may reverse arsenic toxicity on neuronal development.

Differential modulation of host macrophage function by AK-5 tumor is dependent on the site of tumor transplantation.

We have studied the mechanisms involved in the activation or suppression of the immune response by the tumor cells, which is also dependent on the site of tumor transplantation. AK-5 tumor cells when transplanted s.c.

Arsenic induced changes in growth development and apoptosis in neonatal and adult brain cells in vivo and in tissue culture.

Arsenic at a nonlethal level in drinking water consumed over a period of time has been reported to produce chronic toxicity and various types of health problems ranging from skin cancer to disturbance in memory. Neurotoxic effects have been reported in clinical cases with chronic exposure to arsenic. Physiological detoxication of arsenic occurs partially through methylation.