School of Public Health, Zunyi Medical University, Zunyi, Guizhou, 563000, China; An Yang Center for Disease Control and Prevention, Anyang, Henan, 455000, China.
School of Public Health, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Neurotoxicology. 2017 Sep;62:124-129. doi: 10.1016/j.neuro.2017.06.008. Epub 2017 Jun 15.
Occupational and environmental exposure to vanadium has been associated with toxicities in reproductive, respiratory, and cardiovascular systems. The knowledge on whether and how vanadium exposure caused neurobehavioral changes remains incomplete. This study was designed to investigate the changes in learning and memory following drinking water exposure to vanadium, and to conduct the preliminary study on underlying mechanisms. Male Sprague-Dawley rats were exposed to vanadium dissolved in drinking water at the concentration of 0.0, 0.5, 1.0 and 2.0g/L, as the control, low-, medium-, and high- dose groups, respectively, for 12 weeks. The results by the Morris water maze test showed that the time for the testing animal to find the platform in the high exposed group was increased by 82.9% and 49.7%, as compared to animals in control and low-dose groups (p<0.05). There were significantly fewer rats in the medium- and high- dose groups than in the control group who were capable of crossing the platform (p<0.05). Quantitation of vanadium by atomic absorption spectrophotometry revealed a significant dose-dependent accumulation of vanadium in striatum (r=0.931, p<0.01). Histopathological examination further demonstrated a degenerative damage in vanadium-exposed striatum. Interestingly, with the increase of the dose of vanadium, the contents of neurotransmitter ACh, 5-HT and GABA in the striatum increased; however, the levels of Syn1 was significantly reduced in the exposed groups compared with controls (p<0.05). These data suggest that vanadium exposure apparently reduces the animals' learning ability. This could be due partly to vanadium's accumulation in striatum and the ensuing toxicity to striatal structure and synaptic plasticity. Further research is warranted for mechanistic understanding of vanadium-induced neurotoxicity.
职业和环境接触钒与生殖、呼吸和心血管系统的毒性有关。关于钒暴露是否以及如何引起神经行为变化的知识仍然不完整。本研究旨在研究饮用水暴露于钒后学习和记忆的变化，并对潜在机制进行初步研究。雄性 Sprague-Dawley 大鼠分别暴露于浓度为 0.0、0.5、1.0 和 2.0g/L 的饮用水中的钒，作为对照组、低剂量组、中剂量组和高剂量组，分别暴露 12 周。Morris 水迷宫测试的结果表明，高暴露组的测试动物找到平台的时间比对照组和低剂量组增加了 82.9%和 49.7%（p<0.05）。与对照组相比，中剂量组和高剂量组中能够穿过平台的大鼠明显减少（p<0.05）。原子吸收分光光度法定量钒显示，纹状体中钒的积累呈显著剂量依赖性（r=0.931，p<0.01）。组织病理学检查进一步证明了暴露于钒的纹状体有退行性损伤。有趣的是，随着钒剂量的增加，纹状体中神经递质 ACh、5-HT 和 GABA 的含量增加；然而，与对照组相比，暴露组 Syn1 的水平明显降低（p<0.05）。这些数据表明，钒暴露明显降低了动物的学习能力。这可能部分是由于钒在纹状体中的积累以及随后对纹状体结构和突触可塑性的毒性。需要进一步研究以了解钒诱导的神经毒性的机制。
