P-075: Melatonin reduces aluminum induced apoptosis, necrosis and perturbations in the aminergic system of albino mice

Abstract

Monoamine oxidase activity is elevated in certain neurological diseases such as Alzheimer's and Parkinson's disease. Since alterations in monoamines and monoamine oxidase (MAO) have been postulated to play a role in toxic effects of aluminium on the central nervous system, we have attempted to examine the protective effects of melatonin on aluminium induced perturbations in the levels of monoamines and the activity of MAO in albino mice. Two groups of albino mice received intraperitoneal injections of aluminium acetate or melatonin at doses of 3.5 mg/ kg /day and 6 mg/kg/day, respectively, for two weeks. A third group of animals received concurrently aluminium acetate (3.5 mg/kg/day) and melatonin (6mg/kg/day) during the same period. The fourth group of mice were used as control, receiving only distilled water. The animals were killed after 48 hr and the levels of catecholamines, epinephrine, norepinephrine and dopamine and the activity of monoamine oxidase were determined in the cerebellum, hippocampus and cerebral cortex of albino mice. Ultrastructure of cerebellum was also studied by transmission electron microscopy. Aluminium acetate increased the activity of mitochondrial MAO in the tested brain samples. The synaptosomal catecholamines (epinephrine, norepinephrine and dopamine) decreased with aluminium exposure. Aluminium exposure induced cell injury in the cerebellum, apoptosis and necrosis were observed in astrocytes. These results suggest that aluminium- exposure perturbs the aminergic system in the cerebral cortex, cerebellum and hippocampus. Melatonin supplementation significantly reversed the Al-induced perturbations both in the levels of monoamines and in the activity of MAO. Preventive or therapeutic administration of melatonin protected against the induction of aminergic system and cell injury in brain of albino mice treated with aluminium.