Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Belém, State of Pará, Brazil.
Laboratory of Molecular Pharmacology, Institute of Biological Sciences, Federal University of Pará, Belém, State of Pará, Brazil.
Ecotoxicol Environ Saf. 2020 May;194:110358. doi: 10.1016/j.ecoenv.2020.110358. Epub 2020 Mar 6.
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.
铅是一种存在于环境中的有毒金属，具有很大的神经毒性潜力。其主要影响与海马体和小脑损伤有关，导致认知和运动功能障碍，但关于其对脊髓的影响仍缺乏证据。因此，我们旨在研究体内长期接触醋酸铅对大鼠脊髓氧化生物化学和形态的影响。为此，将 36 只雄性 Wistar 大鼠（Rattus norvegicus）分为暴露于 50mg/kg 醋酸铅的实验组和对照组，两组均通过灌胃给予相应处理，持续 55 天。暴露期结束后，处死动物并收集脊髓，进行铅含量定量、丙二醛（MDA）、亚硝酸盐水平等氧化生物化学评估以及抗过氧自由基能力（ACAP）。此外，还进行了形态学评估，包括对成熟和运动神经元的定量分析，以及髓鞘碱性蛋白（MBP）的反应性。我们的结果显示，长期暴露后脊髓中的铅含量较高；ACAP 水平降低；然而，MDA 和亚硝酸盐水平没有差异。此外，三个区域的成熟和运动神经元数量减少，胸腰段的 MBP 免疫标记减少。因此，我们得出结论，长期接触铅能够增加脊髓中的金属水平，影响抗氧化能力，并诱导脊髓实质的形态损伤。我们的结果还表明，铅引发的组织损伤可能是除氧化应激以外的其他分子机制的结果。
