Department of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Egypt.
Neurotoxicology. 2012 Jan;33(1):98-104. doi: 10.1016/j.neuro.2011.12.008. Epub 2011 Dec 16.
Excess manganese (Mn) is potentially toxic resulting in a permanent neurodegenerative disorder, clinically known as "manganism" that is distinctive for hepaticencephalopathy. The present study was designed to explore the toxic impacts of subacute Mn exposure on brain and liver tissues, and the relative abilities of lycopene in averting such neurohepatic damage. Rats were daily injected with MnCl(2) (0 or 6mg/kg, i.p.) 20 days after lycopene administration (0 or 10mg/kg, p.o.), and killed 4 weeks after MnCl(2) exposure. MnCl(2)-induced lipid peroxidation and perturbation in antioxidant system, increase of acetylcholinesterase, aminotransferases, and decrease alkaline phosphatase, and lactate dehydrogenase activities with hyperglycemia as demonstrated by Alzheimer type II astrocytosis, and periportal hepatic necrosis and apoptosis were prevented by lycopene. However, lycopene did not prevent the increased body burden of Mn and the altered Fe and Cu homeostasis induced by MnCl(2). Glutathione S-transferase and catalase activities, and glutathione content were reduced in MnCl(2)-challenged rats, and sustained by lycopene. Our results indicate that although lycopene failed to reduce Mn concentration or retain disturbed elemental status; it appears to be a highly effective in alleviating its neurohepatic deleterious effects by preventing lipid peroxidation, hyperglycemia and changes in the activity of acetylcholinesterase and hepatobiliary enzymes, and antioxidant pathways.
过量的锰（Mn）可能有毒，导致永久性神经退行性疾病，临床上称为“锰中毒”，其特征为肝性脑病。本研究旨在探讨亚急性 Mn 暴露对大脑和肝脏组织的毒性影响，以及番茄红素在避免这种神经肝损伤中的相对能力。MnCl2（0 或 6mg/kg，ip）注射后 20 天给予番茄红素（0 或 10mg/kg，po），4 周后MnCl2 暴露后处死大鼠。MnCl2 诱导的脂质过氧化和抗氧化系统紊乱、乙酰胆碱酯酶、氨基转移酶增加、碱性磷酸酶和乳酸脱氢酶活性降低以及阿尔茨海默病 II 型星形胶质细胞样改变导致的高血糖症、门脉周围肝坏死和细胞凋亡，均被番茄红素所预防。然而，番茄红素并不能预防 MnCl2 引起的 Mn 体负荷增加和 Fe 和 Cu 内稳态的改变。MnCl2 处理的大鼠谷胱甘肽 S-转移酶和过氧化氢酶活性以及谷胱甘肽含量降低，而番茄红素则维持了这些活性。我们的结果表明，尽管番茄红素未能降低 Mn 浓度或维持紊乱的元素状态，但它似乎通过预防脂质过氧化、高血糖和乙酰胆碱酯酶和肝胆酶活性以及抗氧化途径的改变，对其神经肝损伤具有非常有效的缓解作用。
