Long-term exposure to lead reduces antioxidant capacity and triggers motor neurons degeneration and demyelination in spinal cord of adult rats.

Lead is a toxic metal found in environment with great neurotoxic potential. The main effect is associated with impairments in hippocampus and cerebellum, driving to cognitive and motor dysfunctions, however, there is a lack of evidences about the effects over the spinal cord. In this way, we aimed to investigate in vivo the effects of long-term exposure to lead acetate in oxidative biochemistry and morphology of rats' spinal cord. For this, 36 male Wistar rats (Rattus norvegicus) were divided into the group exposed to 50 mg/kg of lead acetate and control group, which received only distilled water, both groups through intragastric gavage, for 55 days. After the exposure period, the animals were euthanized and the spinal cords were collected to perform the analyses of lead levels quantification, oxidative biochemistry evaluation by levels of malondialdehyde (MDA), nitrites and the antioxidant capacity against peroxyl radicals (ACAP). Besides, morphological evaluation with quantitative analysis of mature and motor neurons and reactivity to myelin basic protein (MBP). Our results showed high levels of lead in spinal cord after long-term exposure; there was a reduction on ACAP level; however, there was no difference observed in MDA and nitrite levels. Moreover, there was a reduction of mature and motor neurons in all three regions, and a reduction of immunolabeling of MBP in the thoracic and lumbar segments. Therefore, we conclude that long-term exposure to lead is able of increasing the levels of the metal in spinal cord, affecting the antioxidant capacity and inducing morphological impairments in spinal cord parenchyma. Our results also suggest that the tissue impairments triggered by lead may be resultant from others molecular mechanisms besides the oxidative stress.