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成年 Wistar 大鼠坐骨神经暴露于钒后周围轴突病。

Peripheral axonopathy in sciatic nerve of adult Wistar rats following exposure to vanadium.

机构信息

Neuroscience Unit, Department of Veterinary Anatomy, College of Veterinary Medicine, Federal University of Agriculture, Abeokuta, Nigeria.

Neuroscience Unit, Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.

出版信息

J Peripher Nerv Syst. 2019 Mar;24(1):94-99. doi: 10.1111/jns.12294. Epub 2018 Dec 16.

DOI:10.1111/jns.12294
PMID:30488528
Abstract

Depletion of myelin and neurobehavioural deficits are indications that vanadium crosses the blood-brain barrier and such neurotoxic effects of vanadium on the brain of Wistar rats have been elucidated. The effect however on the peripheral nerves, is yet to be reported. Thus, this work was designed to evaluate the axonal and myelin integrity of sciatic nerves in Wistar rats following exposure to vanadium. Ten male Wistar rats were exposed to 3 mg/kg body weight of sodium metavanadate for 7 days, subjected to rearing and forelimb grip behavioural tests, and sciatic nerves processed for histology (haematoxylin and eosin, cresyl violet, and luxol fast blue). Dystrophic axons with vesiculated myelin, thinned myelin sheath, and demyelinated axons were observed in the vanadium exposed rats, suggestive of axonopathy, classified as fourth-degree nerve injury. Lower behavioural scores were recorded for vanadium-dosed rats; thus, corroborating histological pictures observed of the sciatic nerves. Authors posit that vanadium crossed the "blood-nerve" barrier and caused the observed axonal pathologies and myelin depletion in the sciatic nerves of these rodents with resultant motor deficits. The present paper discusses possible motor deficits and the likely public health importance in regions with crude oil pollution and gas flaring rich in vanadium products.

摘要

髓磷脂耗竭和神经行为缺陷表明钒能够穿过血脑屏障,并且已经阐明了钒对 Wistar 大鼠大脑的这种神经毒性作用。然而,钒对周围神经的影响尚未报道。因此,本研究旨在评估接触钒后 Wistar 大鼠坐骨神经的轴突和髓鞘完整性。10 只雄性 Wistar 大鼠接受 3mg/kg 体重的偏钒酸钠处理 7 天,进行饲养和前肢握力行为测试,并对坐骨神经进行组织学处理(苏木精和伊红、甲苯胺蓝和卢戈氏蓝)。在暴露于钒的大鼠中观察到具有空泡化髓磷脂的变性轴突、髓鞘变薄和脱髓鞘轴突,提示轴突病变,分类为第四级神经损伤。接受钒处理的大鼠的行为评分较低;因此,与观察到的坐骨神经组织学图片相符。作者假设钒穿过“血-神经”屏障,并导致这些啮齿动物的坐骨神经中观察到的轴突病理和髓磷脂耗竭,从而导致运动功能障碍。本文讨论了在富含钒产品的原油污染和天然气燃烧丰富的地区,可能存在的运动功能障碍和对公众健康的重要性。

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