Abstract

Objective: Aluminium (Al) is quite abundant in nature and humans are frequently exposed to Al in daily life. Aluminium salts can exist in different forms and they may have toxic impacts on several tissues including brain. In this study, potential preventive effects of amino-guanidine (AG) (100 mg/kg, i.p.), an inducible nitric oxide synthase inhibitor, on neuron damage to be created by aluminium sulphate (3 mg/kg, i.c.v.) in cerebellar Purkinje cells were determined. Methods: 24 female Wistar albino rats were divided into 4 groups with 6 rats in each: Control (C), Sham (S), Aluminium sulphate ( Al 2 (SO 4 ) 3 ), Aluminium sulphate + Amino-guanidine ( Al 2 (SO 4 ) 3 +AG). A single aluminium sulphate (3 mg/kg) dose dissolved in 0.9% NaCl was injected intracerebroventricularly to aluminium sulphate and aluminium sulphate + amino-guanidine groups at the beginning of experiments. Following aluminium sulphate injection, amino-guanidine (100 mg/kg) dissolved in distilled water was injected to aluminium sulphate + amino-guanidine group intraperiteonally for 15 days. Nothing was administered to control group, a single dose of 0.9% (3 mg/kg, i.c.v.) sodium chloride (NaCl) was administered to sham group at the beginning of experiments. Cerebellum tissues of the rats were removed 15 days after treatments and they were assessed histopathologically and stereologically. Results: Stereological optic fractionation method revealed cerebellar total number of Purkinje cells as 417615±16238,8 in control group; 378650±20171,6 in Sham group; 272945±15499,5 in Aluminium sulphate group; 324581±16324,8 in Aluminium sulphate + Amino-guanidine group. Conclusion: It was concluded based on present findings that amino-guanidine reduced aluminium induced Purkinje cell loss through nitric oxide synthase (NOS) inhibition.

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