Induction of oxidative stress by non-lethal dose of mercury in rat liver: possible relationships between apoptosis and necrosis.

Sprague Dawley strain of male rats weighing 200 +/- 10.0 g, were exposed intramuscularly to non-lethal dose of mercury for short acute duration of 24 and 48 hr. Mercury treatment increased thio-barbituric acid reactive substance (TBARS) and conjugated diene (CD) content with increase in duration when compared with control. This reflects possible increase in lipid peroxidation, revealing that sufficient intoxication was generated by non-lethal dose of mercury. Furthermore, mercury treatment decreased tissue glutathione (GSH) content to 2.07 and 1.49 microg GSH mg protein(-1) with concomitant decrease in glutathione-S-transferase (GST) activity by 26.06 and 36.40% after 24 and 48 hr of exposure respectively. The elevations of aspartate transaminase (AST) and alanine transaminase (ALT) levels measured exhibited increase of 287.5 and 214.5% after 48 hr of exposure respectively which were found to be highly significant compared with control. Western blot analysis indicated upregulation of caspase-9 and upsurge in effect or caspase-3 activity leading to apoptosis. The concluded findings of the present investigation suggests possible role of early mercury exposure in inducing oxidative stress mediated apoptosis in mammalian model systems as an indicator component of environmental toxicology.