AUGMENTATION OF CHRYSOTILE-INDUCED OXIDATIVE STRESS BY BHA IN MICE LUNGS

Asbestos is known to induce oxidative stress in the lung. The consumpt ion of butylated hydroxyanisole (BHA) in preserved food and soft drink s is increasing in the general population, which includes workers in a sbestos factories. Because there is no information on the effect of co -exposure to chrysotile and BHA, the time-dependent effects of a singl e intratracheal dose of chrysotile (1 mg per mouse) and a single ip do se of BHA (350 mg/kg body weight) on various indices of oxidative stre ss such as lipid peroxidation, hydrogen peroxide generation, glutathio ne peroxidase (GPX), glutathione reductase (GR), catalase, glucose-6-p hosphate dehydrogenase (G6PDH) and glutathione (GSH) were followed for up to 14 days. Microsomal lipid peroxidation (as well as that induced by NADPH) was significantly enhanced by BHA in the chrysotile-exposed group. GPX and GR activities in the same group were gradually decreas ed by BHA. Non-significant modulation of catalase activity by BHA was also noted. BHA induces GSH to a significant extent in lungs exposed w ith chrysotile. An increase in the G6PDH activity was maximal (19%; P < 0.05) at day 3. The results clearly demonstrate that BHA enhances ch rysotile-induced oxidative stress in the lung.