溴氰菊酯对大鼠神经系统的氧化应激作用

目的　观察溴氰菊酯(DM)在大鼠大脑皮层和海马组织诱导的脂质过氧化作用。方法　DM3.12 5、12 .5 0 0mg/kg染毒大鼠,测定其大脑皮层和海马组织丙二醛(MDA)水平和总超氧化物歧化酶(T SOD ,包括Mn SOD和CuZn SOD)、过氧化氢酶(CAT)、谷胱甘肽S 转移酶(GST)、谷胱甘肽过氧化物酶(GSH Px)和谷胱甘肽还原酶(GR)活力。脑组织细胞质碎片γ谷氨酰半胱氨酸合成酶(γGCS)活力和GSH含量用OPA柱前衍生反相高效液相色谱荧光法检测。结果　DM染毒5d ,(1) 12 .5 0 0mg/kgDM组大鼠大脑皮层MDA含量高于3.12 5mg/kgDM组,海马MDA含量高于对照组和3.12 5mg/kgDM组。(2 )两组DM染毒大鼠大脑皮层T SOD和CuZn SOD活力均低于对照组,差异均有统计学意义(P <0 .0 1或P <0 .0 5 )。(3) 12 .5 0 0mg/kgDM组大鼠大脑皮层GSH含量高于对照组,海马GSH含量低于对照组和3.12 5mg/kgDM组;3.12 5mg/kgDM组大鼠大脑皮层GR活力[(11.80±5 .15 )U/mgpro]低于对照组和12 .5 0 0mg/kgDM组[(18.98±3.6 8)、(17.35±2 .4 7)U/mgpro],3.12 5、12 .5 0 0mg/kgDM组大鼠海马GR活力[(2 1.4 6±8.89)、(2 1.6 3±4 .92 )U/mgpro]均低于对照组[(31.2 2±6 .97)U/mgpro];12 .5 0 0mg/kgDM组海马γGCS活力[(1.75±0 .6 0 )nmol·mgpro-1·min-1]低于对照组和

Oxidative stress of deltamethrin on rat nervous system

OBJECTIVE: To explore the lipid peroxidation induced by deltamethrin (DM) in the cerebral cortex and hippocampus of rat. METHODS: Wistar male rats were administrated with DM (daily dose was 3.125, 12.500 mg/kg respectively). The content of malondialdehyde (MDA) and the activity of total-superoxide dismutase (T-SOD, including Mn-SOD and CuZn-SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) in cerebral cortex and hippocampus tissue were determined. The reduced glutathione (GSH) content and gamma-glutamylcysteine synthetase (gamma-GCS) activity in cytosolic fraction of cerebral cortex and hippocampus tissue was determined by reversed-phase high performance liquid chromatographic assay with o-phthalaldehyde pre-column derivation. RESULTS: (1) MDA content in cerebral cortex of the high dose group was significantly higher than those in the low dose group, and MDA content in hippocampus tissue of the high dose group was significantly higher than those in both the control and the low dose group after 5 d of DM exposure. (2) The activity of T-SOD and CuZn-SOD in cerebral cortex of both high and low dose group were significantly lower than that in the control group, and there was no effect on CAT activity in cerebral cortex (P < 0.01 or P < 0.05). (3) GSH content in cerebral cortex of the high dose group was significantly higher than that in control group (P < 0.05), and that in hippocampus tissue of high dose was significantly lower than that in both control and low dose group (P < 0.05). GR activity of low dose group in cerebral cortex was significantly lower than that in both control and high group [(11.80 +/- 5.15) vs (18.98 +/- 3.68), (17.35 +/- 2.47) U/mg pro] (P < 0.01). Gamma-GCS activity in hippocampus tissue of the high dose group was significantly lower than that in both control and low dose group [(1.75 +/- 0.60) vs (3.17 +/- 0.79), (2.72 +/- 0.75) nmol x mg pro(-1) x min(-1)] (P < 0.01). GR activity in hippocampus tissue of both high and low dose group was significantly lower than that in the control group [(21.63 +/- 4.92), (21.46 +/- 8.89) vs (31.22 +/- 6.97) U/mg pro] (P < 0.05). CONCLUSION: The oxidative stress in nerve tissue, which could be resulted from effect of DM on the activity of SOD, gamma-GCS and GR and GSH content, is one of the mechanisms of neuro-toxicity induced by DM; The decreased activity of gamma-GCS and GR may be the primary cause of DM-induced decrease in that GSH content in hippocampus tissue.