Alterations in glutathione system in adult and pup rat brains following chronic aluminum exposure

Glutathione is a major regulator of the redox equilibrium in cells, so its deficit weakens the tissue resistance to oxidants. Several pathologies that affect the nervous system involve oxidative stress, possibly associated with the decrease of glutathione content. The nervous system is particularly susceptible to oxidative insults and is therefore dependent on its glutathione content, especially during development stage, where brain metabolism and growth are maximal. To study the involvement of glutathione in brain redox homeostasis, we set up an experimental model of aluminum (Al) neurotoxicity (AlCl3+ 100 mg/kg b.wt) for eight weeks to both developed and developing rats. In the developing group exposure of Al for 60 days was done post natally, 21 days to feeding mother (lactation period) and 39 days to pup rats. Similar dose for eight weeks were given to adult rats. The result showed a statistically significant ( P < 0.01) decrease in Total glutathione, reduced glutathione and oxidized glutathione in both cerebrum and cerebellum region of pup brains. A similar decrease was observed in adult group. Also, aluminum exposure resulted in significant decrease in ATPase activity in both the regions of the brain of developing and developed rat brain. Thus the present study indicates that aluminum exposure (100 mg/kg b.wt) to both adult and pup rat results in the decline of glutathione system which alters the redox ratio significantly. Further, aluminum exposure also decreases the ATPase activity which in turn could affect the glutathione synthesis.