Abstract
Background: Aluminum enters human body through food and drinking, cosmetics, and occupational exposures. Aluminum (Al) is a highly neurotoxic element causes neuronal degeneration in humans as well as in animals. Studies reported that Bacopa monnieri has anxiolytic, antidepressant, antioxidant, and memory-enhancing property. Hexokinase is a very important glycolytic enzyme and also rate-limiting enzyme determines the rate of glucose utilization by the cells.

Aims and Objectives: The study was planned to investigate whether Al exposure affects the hexokinase activity and protective effect of Bacopa on hexokinase activity in discrete regions of brain and other vital organs.

Materials and Methods: Wistar albino rats were divided into four groups, each group consists of six. Group 1 as control received distilled water, Group 2 received Al chloride, Group 3 received crude extract of Bacopa, and Group 4 received Al as well as Bacopa. After 30 days of Al and Bacopa administration, rats were sacrificed, tissues were homogenized and hexokinase was assayed.

Results: In all the tissues (liver, muscle, kidney, cerebral cortex, hippocampus, and cerebellum), Al treated as well as Al + Bacopa-treated animals showed significant decrease in hexokinase activity when compared with control animals. However, the Bacopa and Al-treated animals showed a marked increase in the hexokinase activity from Al alone treated animals. Moreover, no change in hexokinase activity was observed between control and Bacopa-treated animals.

Conclusion: Al affects the hexokinase activity whereas, Bacopa enhances the hexokinase activity by inhibiting the toxic effects of Al.