Lab. of Cell Engineering & 3-D Structure, School of Life Sciences and Biotechnology, Korea University, Seoul, 136-701, Korea.
Toxicol Mech Methods. 2005;15(6):399-404. doi: 10.1080/15376520500194742.
Cypermethrin is a potent pesticide derived from natural pyrethrin of the chrysanthemum plant. Cypermethrin has been known to modulate the blood-brain barrier and induce oxidative stress in rats. The oxidative stresses leading to increased reactive oxygen species generation have been identified within the degeneration of the dopaminergic (DA) neuron. However, in testing cypermethrin for its relationship to the degeneration of DA neurons, an experimental study has not yet been done. This study was designed to investigate the effects of cypermethrin on the DA neurons in the substantia nigra of normal and progressive hemiparkinsonian rats. The degree of degeneration of DA neurons was evaluated by tyrosine hydroxylase (TH) immunohistochemistry and forepaw adjusting step (FAS) test. The administration of cypermethrin (15 and 75 mg/kg/day) to the normal rats for 15 days did not decrease the number of TH-immunopositive (TH-IP) DA neurons in the substantia nigra. However, the low dose (15 mg/kg/day) of cypermethrin enhanced the rate of decline of DA neurons in the substantia nigra of hemiparkinsonian rats at 10 days and 3 weeks (p < 0.05). Also, the number of FAS in cypermethrin-treated hemiparkinsonian rats was reduced more rapidly than that of cypermethrin not-treated hemiparkinsonian rats at 10 days, 3 weeks, and 6 weeks (p < 0.05). These results suggest that cypermethrin per se cannot directly induce the degeneration of DA neurons but can accelerate a toxic effect on the degeneration of DA neurons in the progressive hemiparkinsonian rats.
氯菊酯是一种从菊花植物中天然除虫菊衍生而来的强效农药。已知氯菊酯可以调节血脑屏障并在大鼠中诱导氧化应激。在多巴胺能 (DA) 神经元变性中，已经确定导致活性氧 (ROS) 生成增加的氧化应激。然而，在测试氯菊酯与 DA 神经元变性的关系时，尚未进行实验研究。本研究旨在探讨氯菊酯对正常和进行性半帕金森大鼠黑质 DA 神经元的影响。通过酪氨酸羟化酶 (TH) 免疫组织化学和前爪调节步 (FAS) 试验评估 DA 神经元变性程度。氯菊酯 (15 和 75 mg/kg/天) 连续 15 天给药正常大鼠并未降低黑质中 TH 免疫阳性 (TH-IP) DA 神经元的数量。然而，低剂量 (15 mg/kg/天) 的氯菊酯在 10 天和 3 周时增强了半帕金森大鼠黑质中 DA 神经元的下降速度 (p < 0.05)。此外，与未用氯菊酯治疗的半帕金森大鼠相比，用氯菊酯治疗的半帕金森大鼠的 FAS 数量在 10 天、3 周和 6 周时更快地减少 (p < 0.05)。这些结果表明，氯菊酯本身不能直接诱导 DA 神经元变性，但可以加速进行性半帕金森大鼠中 DA 神经元变性的毒性作用。
