This preclinical animal study in adult male rats investigated whether selenium supplementation could mitigate lead-induced brain damage.
Scientific Reports · 4 authors, 2 centres
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This preclinical animal study in adult male rats investigated whether selenium supplementation could mitigate lead-induced brain damage.
The study used a preclinical animal model of adult male rats to evaluate the neuroprotective effects of selenium against lead-induced neurotoxicity. Central results indicated that lead exposure (both low and high doses) significantly reduced body and brain weights, increased oxidative stress (elevated MDA, decreased TAC), caused cerebral DNA fragmentation, and led to histological and ultrastructural damage in the cerebrum. Co-administration of selenium with lead significantly ameliorated these detrimental effects, as evidenced by improvements in weight parameters, oxidative stress markers, DNA damage, and histopathological scores, particularly in the low Pb + Se group which showed near-normal cortical thickness and neuron counts. Limitations include the use of an animal model with indirect human relevance, the study's focus on only the cerebrum, and the need for further dose-finding studies. The implications are that selenium has a potential protective role against lead neurotoxicity via modulation of oxidative stress and apoptosis pathways, though this is not established as a human treatment recommendation.