722-730The present
study was designed to analyze the effect of acute aluminium phosphide (ALP) (10
mg/kg body wt.) exposure on the glucose homeostasis in rat liver and brain. ALP
has been implicated in the inhibition of cytochrome oxidase causing reduced
oxygen uptake and decreased ATP synthesis eventually resulting in cellular
energy crisis. A significant decrease in plasma glucose levels in the ALP
treated rats has been observed. Therefore, decreased ATP levels coupled with
hypoglycemia may further intensify the cellular energy deficits. In order to
meet the sudden increase in the local energy demand, the brain tissue utilizes
its stored energy in the form of glycogen breakdown as observed by a decrease in
the glycogen levels in both liver and brain which was accompanied by a marked
increase in the activity of glycogen phosphorylase in both the tissues. The
glycolytic rate was found to be enhanced in brain tissue as evident by
increased activities of hexokinase and phosphofructokinase enzymes, but
decreased in liver of ALP treated rats. Lactate levels were increased in plasma
and brain, but decreased in liver of ALP treated rats. Pyruvate levels
increased in the plasma and liver, but no change was observed in the brain
tissue. ALP did not cause any change in the gluconeogenic enzymes like
glucose-6-phosphatase and fructose-1,6-bisphophatase in brain, but a
significant increase was observed in the liver. Results of the study showed
that ALP induced cellular energy deficit leads to compromised energy status of
liver and brain coupled with substantial alterations in glucose homeostasis.
However, the activity of glucose-6-phosphate dehydrogenase decreased
significantly in both the tissues