Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
Department of Medical Laboratory Science, Ladoke Akintola University, Oshogbo, Nigeria.
Metab Brain Dis. 2018 Apr;33(2):377-385. doi: 10.1007/s11011-017-0070-9. Epub 2017 Jul 25.
Vanadium is known to induce reactive oxygen species (ROS) in biological systems. Exposure to vanadium has been linked to neurological defects affecting the central nervous system (CNS) early in life and culminates later to neurodegeneration. This study was designed to evaluate the effects of chronic vanadium exposure on antioxidant profile in mice, and progressive changes after withdrawal from treatment. A total of 85 male BALB/c mice (4 weeks old) were used for the experiment and were divided into three groups of vanadium exposed (3 mg/kg i.p at 3-18 months treatment), matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn. Vanadium exposure caused significant increases (p<0.05) in levels of malondialdehyde (MDA), hydrogen peroxide (HO) generation and nitric oxide with a concomitant decrease (p<0.05) in the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase and a decline in the level of reduced glutathione (GSH) after 6 months of vanadium exposure in the brain. This trend continued in all vanadium-exposed groups (9, 12, 15 and 18 months) relative to the matched controls. Withdrawal after 3 months of vanadium exposure significantly reversed oxidative stress in intoxicated mice from 9 to 15 months after vanadium withdrawal. We have shown that chronic administration of vanadium led to oxidative stress in the brain which is reversible only after a long period of vanadium withdrawal.
钒被认为会在生物系统中诱导活性氧（ROS）。暴露于钒已与影响中枢神经系统（CNS）的神经缺陷有关，这些缺陷在生命早期出现，并在后期导致神经退行性变。本研究旨在评估慢性钒暴露对小鼠抗氧化谱的影响，以及停止治疗后逐渐发生的变化。总共使用了 85 只雄性 BALB/c 小鼠（4 周龄）进行实验，并将其分为三组：钒暴露组（3 毫克/千克腹腔注射，治疗 3-18 个月）、匹配对照组和暴露于钒三个月后停止治疗的动物组。钒暴露导致丙二醛（MDA）、过氧化氢（HO）生成水平显著升高（p<0.05），同时超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽-S-转移酶的活性降低（p<0.05），以及还原型谷胱甘肽（GSH）水平降低，在大脑中暴露于钒 6 个月后出现这种趋势。这种趋势在所有暴露于钒的组（9、12、15 和 18 个月）中都持续存在，与匹配对照组相比。停止暴露 3 个月后，在钒暴露后 9 至 15 个月，中毒小鼠的氧化应激显著逆转。我们已经表明，慢性给予钒会导致大脑中的氧化应激，只有在长时间停止钒暴露后才能逆转。
