The mitigating effect of selenium against lead-induced neurotoxicity in the cerebellar cortex of adult male albino rats

Lead (Pb)-induced neurotoxicity is a major public health problem. The nervous system is the primary target of Pb toxicity. Since selenium (Se) has anti-inflammatory and antioxidant effects that have been shown to provide some protection against heavy metal toxicity, the present study aimed to demonstrate the potential protective role of Se against the effects of Pb on the cerebellar structure of rats using histopathological, immunohistochemical, biochemical and molecular measures. Experimental rats were divided into 3 groups, each divided into 2 subgroups: control group (Se-free and Se-supplemented subgroups), Pb group (low and high dose Pb subgroups), and Pb/Se group (low and high dose Pb subgroups with Se). After 4 weeks of administration, cerebellar samples were collected for investigation.  Pb-induced cerebellar damage was manifested by significant increases in the glial fibrillary acidic protein (GFAP), brain oxidative marker (malondialdehyde) and apoptosis (DNA fragmentation), particularly at high dose. Pb also caused alteration of normal cerebellar structure and cellular degeneration with a significant reduction in the total number of Purkinje cells and the thickness of molecular and granular layers. All these alterations were greatly mitigated by co-administration of Se especially in the low dose Pb/Se subgroup. Se has been suggested to reduce Pb-induced neurotoxicity in the cerebellum. Further experimental studies are recommended before applying the results in clinical trials.