College of Life Science and Oceanography, Shenzhen University, Shenzhen 518060, PR China; School of Public Health, the key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang 550025, PR China.
Shenzhen Customs Food Inspection and Quarantine Technology Centre, Shenzhen 518000, PR China.
J Trace Elem Med Biol. 2023 Dec;80:127289. doi: 10.1016/j.jtemb.2023.127289. Epub 2023 Aug 23.
Exposure to arsenic (As) is a major public health challenge worldwide. Chronic exposure to As can cause various human health effects, including skin diseases, cardiovascular disease, neurological disorders, and cancer. Studies have shown that As exposure can lead to disturbances in the balance of trace elements in the body. Moreover, As readily crosses the blood-brain barrier and can be enriched in the hippocampus and cortex, causing neurotoxic damage. At present, there are few reports on the effect of As on trace element levels in the central nervous system (CNS). Therefore, we sought to explore As-induced neurotoxicity and the effects of As on CNS trace element levels.
An As-induced neurological injury model in rats was established by feeding As chow for 90 days of continuous exposure, and 19 elements were detected in the hippocampus and cortex of As-exposed rats by inductively coupled plasma mass spectrometry.
The results showed that the As levels in the hippocampus and cortex of As-exposed rats were significantly higher than those in the control group, The As levels in the cortex were significantly higher than in the hippocampus group. The levels of Cd, Ho, and Rb were increased in the hippocampus and decreased in Au, Ba, Ce, Cs, Pd, Se, Sr, and Tl in the As-exposed group, while the levels of Cd and Rb were increased and Se and Au were decreased in the cortex. Significant gender differences in the effects of As on hippocampal Cd, Ba, Rb, and Sr, and cortical Cd and Mo.
It is suggested that elemental imbalance may be a risk factor for developing As toxicity plays a synergistic or antagonistic role in As-induced toxicity and is closely related to As-induced CNS damage.
暴露于砷（As）是全球主要的公共卫生挑战。慢性暴露于 As 会导致各种人类健康影响，包括皮肤病、心血管疾病、神经紊乱和癌症。研究表明，As 暴露会导致体内微量元素平衡失调。此外，As 很容易穿过血脑屏障，并在海马体和皮质中富集，导致神经毒性损伤。目前，关于 As 对中枢神经系统（CNS）中微量元素水平的影响的报道很少。因此，我们试图探讨 As 诱导的神经毒性和 As 对 CNS 微量元素水平的影响。
通过连续暴露 90 天喂食 As 饲料，建立大鼠砷诱导的神经损伤模型，通过电感耦合等离子体质谱法检测 As 暴露大鼠海马体和皮质中的 19 种元素。
结果表明，As 暴露大鼠海马体和皮质中的 As 水平明显高于对照组，皮质中的 As 水平明显高于海马体组。在 As 暴露组中，海马体和皮质中的 Cd、Ho 和 Rb 水平升高，Au、Ba、Ce、Cs、Pd、Se、Sr 和 Tl 水平降低，而 Cd 和 Rb 水平在皮质中升高，Se 和 Au 水平降低。As 对海马体 Cd、Ba、Rb 和 Sr 以及皮质 Cd 和 Mo 的影响存在显著的性别差异。
提示元素失衡可能是砷毒性发病的危险因素，在砷诱导的毒性中发挥协同或拮抗作用，与砷诱导的中枢神经系统损伤密切相关。
