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.

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To accurately know the time-dependent changes of the lipid peroxidation and antioxidative status for elucidating the mechanism of neuropathy induced by allyl chloride (AC), the malondialdehyde (MDA), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) were investigated in cerebrum, spinal cord and sciatic nerve of rats after 0, 3, 6, 9, 12 weeks of AC administration. AC was administrated to Wistar rats by gavage at a single dosage of 200 mg/kg/per dose (three times per week). Rats were sacrificed after 0, 3, 6, 9, 12 weeks of treatment, and cerebrum, spinal cord, sciatic nerves were dissected, homogenized and used for the determination of lipid peroxidation and antioxidative status. The results showed that MDA in cerebrum (112.4%) and sciatic nerve (113.1%) significantly increased (P<0.05) on third week of AC treatment and at gait score of 2, and further changes of MDA were observed after 6, 9, 12 weeks and at gait score of 3, 4. While a decrease (P<0.05) in the activities of GSH, CAT, GPx and SOD after 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4 were observed in cerebrum, spinal cord and sciatic nerve. Anti-ROS activities also decreased in all three nerve tissues after 3, 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4. Thus, AC intoxication was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time-dependent changes of these indexes in Wistar rats nerve tissues occurred. Sciatic nerve was the main target tissue and MDA was most sensitive among all indexes. The changes of lipid peroxidation and antioxidative status might be related to the degradation of nerve fiber and served as one of mechanisms of toxic neuropathy induced by AC.

To investigate the mechanism of carbon disulfide-induced neuropathy, male Wistar rats were randomly divided into two experimental groups and one control group. The rats in two experimental groups were treated with carbon disulfide by gavage at dosages of 300 and 500 mg/kg/day, respectively, five times per week for 12 weeks. Spinal cords of carbon disulfide-intoxicated rats and their age-matched controls were Triton-extracted and ultracentrifuged to yield a pellet fraction of neurofilament (NF) polymer and a corresponding supernatant fraction. Then, the contents of NF triplet proteins (NF-H, NF-M, NF-L) and two calpain isoforms (m-calpain and mu-calpain) in both fractions were determined by immunoblotting. In the meantime, the mRNA levels of NF-H, NF-M, and NF-L in spinal cords were quantified using reverse transcriptase-polymerase chain reaction. Results showed that in the pellet fraction, the contents of three NF subunits in both treated groups decreased significantly except NF-L in low dose group. In the supernatant fraction, the pattern of NFs alteration varied according to dose-levels. Compared to controls, three neurofilmant subunits in the high dose group displayed significant reduction consistently. However, in the low dose group, they remained unaffected. As for calpains, the contents of mu-calpain in both fractions increased significantly regardless of carbon disulfide dose-levels. Meanwhile, m-calpain demonstrated a significant decline in the supernatant fraction, and remained unchangeable in the pellet fraction compared to the control group. Furthermore, the levels of mRNA expression of NF-H, NF-M, and NF-L genes were elevated consistently in CS(2)-treated groups. These findings suggested that carbon disulfide intoxication was associated with obvious alterations of NFs content in rat spinal cord, which might be involved in the development of carbon disulfide neurotoxicity.