Nicotine neuronal interactions exert an adverse potential in some brain regions and a significant link has been established between tobacco smokeicotine and vascular impairment. This work addresses nicotine impact on various components of the substantia nigra compacta (SNc) in rat. Twenty adult male Albino rats were divided equally into two groups: Group I, vehicle-control group (received saline [1 ml/kg body weight intra peritoneally] for 11 days). Group II; nicotine group (received 1.5 mg/kg body weight/day Sc) for 11 days. Nicotine levels were detected in the serum. Specimens were taken from the mid brain, processed and examined using biochemical, immunohistochemical, ultrastructural and morphometric techniques. In nicotine group, biochemical analysis revealed reduction in total antioxidant capacity (TAC), decrease in dopamine and malondialdehyde (MDA) levels. The mean number of light cells, and the mean surface area of nerve cells/field were significantly reduced, with an increase of dark cells were found in nicotine group compared to control.Immunoreactivity in nicotine group revealed an increase in neuronal α-synuclein, reduction in tyrosine hydroxylase enzyme, an increase in caspase 3 and ultrastructure changes suggestive of neuronal apopto. The blood capillaries were markedly affected. Nicotine induced endothelial and pericytic apoptotic changes, irregular lumena and indistinct endothelial junctional complex. Nicotine administered subcutaneously in a small dose may have a deleterious effect on SNc, mainly involving dopaminergic neurons and blood capillaries. This effect seems to be secondary to an oxidative stress that might be produced by reduced TAC and increased MDA levels.

Nicotine neuronal interactions exert an adverse potential in some brain regions and a significant link has been established between tobacco smokeicotine and vascular impairment. This work addresses nicotine impact on various components of the substantia nigra compacta (SNc) in rat. Twenty adult male Albino rats were divided equally into two groups: Group I, vehicle-control group (received saline [1 ml/kg body weight intra peritoneally] for 11 days). Group II; nicotine group (received 1.5 mg/kg body weight/day Sc) for 11 days. Nicotine levels were detected in the serum. Specimens were taken from the mid brain, processed and examined using biochemical, immunohistochemical, ultrastructural and morphometric techniques. In nicotine group, biochemical analysis revealed reduction in total antioxidant capacity (TAC), decrease in dopamine and malondialdehyde (MDA) levels. The mean number of light cells, and the mean surface area of nerve cells/field were significantly reduced, with an increase of dark cells were found in nicotine group compared to control.Immunoreactivity in nicotine group revealed an increase in neuronal α-synuclein, reduction in tyrosine hydroxylase enzyme, an increase in caspase 3 and ultrastructure changes suggestive of neuronal apopto. The blood capillaries were markedly affected. Nicotine induced endothelial and pericytic apoptotic changes, irregular lumena and indistinct endothelial junctional complex. Nicotine administered subcutaneously in a small dose may have a deleterious effect on SNc, mainly involving dopaminergic neurons and blood capillaries. This effect seems to be secondary to an oxidative stress that might be produced by reduced TAC and increased MDA levels.