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Effects of acrylamide on the nervous tissue antioxidant system and sciatic nerve electrophysiology in the rat.

机译:丙烯酰胺对大鼠神经组织抗氧化系统和坐骨神经电生理的影响。

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摘要

To investigate the time-dependent effects of acrylamide (ACR) on the antioxidative status in rat nerve tissues, adult male Wistar rats were given ACR (40 mg/kg, i.p., 3 times/week) for 2, 4, 6 and 10 weeks, respectively. The time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues were investigated. The electrophysiology indices (nerve conduction velocity, NCV; compound action potential duration, CAPD; compound action potential amplitude, CAPA; compound action potential latency, CAPL) in the sciatic nerve were determined using BL-420E Biologic Function Determining System. The results showed that MDA levels increased significantly (P < 0.05) in nerve tissues, while GSH levels markedly decreased (P < 0.05) in a time-dependent manner. SOD activity (in the spinal cord and sciatic nerve) and GR activity (in the sciatic nerve) increased significantly after 4 weeks ACR treatment (P < 0.01), but then decreased (P < 0.05). The anti-ROS activity in the sciatic nerve was markedly decreased at the end of week 6 and 10 (P < 0.01). The above indices changed most in the sciatic nerve. The levels of GSH, MDA and anti-ROS in rat sciatic nerve were in high correlation (P < 0.05, |r| > 0.80) with the electrophysiology indices according to the exposure time. Thus, ACR-induced neurotoxicity may be associated with the enhancement of lipid peroxidation and reduction of the antioxidative capacity. Depletion of neural GSH level might be one of the primary events in ACR-induced neuropathy.
机译:为了研究丙烯酰胺(ACR)对大鼠神经组织抗氧化状态的时间依赖性影响,对成年雄性Wistar大鼠给予ACR(40 mg / kg,腹腔注射,每周3次,每周2、4、6和10周) , 分别。脂质过氧化(丙二醛,MDA)和抗氧化状态(谷胱甘肽,GSH;谷胱甘肽过氧化物酶,GSH-Px;谷胱甘肽还原酶,GR;超氧化物歧化酶,SOD和抗活性氧,抗ROS)随时间的变化检查神经组织。使用BL-420E生物功能测定系统测定坐骨神经的电生理指标(神经传导速度,NCV;复合动作电位持续时间,CAPD;复合动作电位振幅,CAPA;复合动作电位潜伏期,CAPL)。结果显示神经组织中的MDA水平显着增加(P <0.05),而GSH水平显着下降(P <0.05)。 ACR治疗4周后,SOD活性(在脊髓和坐骨神经中)和GR活性(在坐骨神经中)显着增加(P <0.01),然后下降(P <0.05)。在第6周和第10周末,坐骨神经中的抗ROS活性明显降低(P <0.01)。上述指标在坐骨神经中变化最大。根据接触时间,大鼠坐骨神经中GSH,MDA和抗ROS的水平与电生理指标高度相关(P <0.05,| r |> 0.80)。因此,ACR诱导的神经毒性可能与脂质过氧化作用的增强和抗氧化能力的降低有关。神经GSH的水平降低可能是ACR诱发的神经病的主要事件之一。

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