Opacka J, Opalska B, Kołakowski J, Wrońska-Nofer T
Toxicol Lett. 1986 Jul-Aug;32(1-2):9-18. doi: 10.1016/0378-4274(86)90043-3.
Neurotoxic effects of the combined exposure of rats to carbon disulphide (CS2) and ethanol (EtOH) were studied. Biochemical and ultrastructural evaluation of the central nervous system (CNS) and peripheral nervous system (PNS) was performed. Male Wistar rats were exposed to CS2 vapour (0.8 mg/l air) and to 10% alcohol in the drinking water for 8 months. EtOH elevated the increase in beta-glucuronidase activity caused by CS2 in the hippocampus and in the cerebral cortex. No effect on the high-affinity synaptosomal uptake of L-glutamate and GABA was observed and no marked ultrastructural changes in the tested brain regions were found. In the peripheral nerves CS2 alone evoked axonal degeneration whereas CS2 combined with EtOH caused disturbances in myelin. Ultrastructural changes preceded biochemical alterations in the PNS and the biochemical indicators of peripheral neuropathy such as beta-glucuronidase activity and cholesterol ester content were not significantly affected. It is suggested that CS2 and EtOH combined affect both PNS and CNS to a higher extent than each of these substances alone.
研究了大鼠联合暴露于二硫化碳（CS2）和乙醇（EtOH）的神经毒性作用。对中枢神经系统（CNS）和外周神经系统（PNS）进行了生化和超微结构评估。将雄性Wistar大鼠暴露于CS2蒸气（0.8毫克/升空气）和饮用水中的10%酒精中8个月。乙醇加剧了CS2导致的海马体和大脑皮层中β-葡萄糖醛酸酶活性的增加。未观察到对L-谷氨酸和GABA的高亲和力突触体摄取有影响，并且在测试的脑区未发现明显的超微结构变化。在周围神经中，单独的CS2引起轴突变性，而CS2与乙醇联合导致髓鞘紊乱。超微结构变化在外周神经系统的生化改变之前出现，并且外周神经病变的生化指标如β-葡萄糖醛酸酶活性和胆固醇酯含量未受到显著影响。提示CS2和乙醇联合对PNS和CNS的影响程度高于单独使用这两种物质中的任何一种。
