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首页> 外文期刊>Journal of applied toxicology >Response of the olfactory bulb antioxidant system following diethyldithiocarbamate (DDTC) administration in rats.
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Response of the olfactory bulb antioxidant system following diethyldithiocarbamate (DDTC) administration in rats.

机译：大鼠二乙基硫代氨基甲酸乙酯（DDTC）给药后嗅泡抗氧化体系的响应。

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摘要

This study was designed in order to evaluate alterations in the reactive oxygen species (ROS) scavenging system in olfactory bulb, dorsal neocortex and cerebellum for 6 weeks following a single subcutaneous dose (600 mg kg-1) of diethyldithiocarbamate (DDTC) to rats. A single dose of DDTC caused substantial damage to the olfactory epithelium and degeneration within the olfactory bulb. The epithelium regenerates, followed by regeneration in the olfactory bulb. The mean olfactory bulb weight decreased significantly 3 days after DDTC administration and gradually recovered to control values in 6 weeks. The DDTC-induced lesion of the olfactory nerve resulted in significant changes in glutathione (GSH) and antioxidant enzyme activities in olfactory bulb. In contrast, no significant changes were found in either cerebellum or dorsal neocortex. These observations indicate that a single dose of DDTC selectively affected the ROS scavenging system of the olfactory bulb. Moreover, these changes persisted for at least 6 weeks, which includes regeneration and synaptogenesis. Olfactory bulb GSH concentrations decreased significantly by 47 +/- 4%, glutathione reductase activity decreased by 18 +/- 3% and catalase activity increased by 27 +/- 7% over the 6 weeks. Superoxide dismutase activity decreased significantly in olfactory bulb of rats by 32 +/- 6% at 3 days following the lesion and then recovered and increased by 38 +/- 3% at 3 weeks. Olfactory bulb malondialdehyde concentrations were elevated (298 +/- 67%) throughout the post-lesion survival period, although this change did not reach the stringent statistical significance level required in this study. These data suggest that increased ROS flux perturbs the olfactory bulb antioxidant defense system during olfactory nerve regeneration.
机译：设计了该研究，以评估嗅泡（ROS）清除系统中的反应性氧气种类（ROS）清除系统的改变，在单一皮下剂量（600mg KG-1）二乙基硫代氨基甲酸乙酯（DDTC）至大鼠后6周。单剂量的DDTC对嗅灯泡内的嗅性上皮和变性引起了大量损伤。上皮再生，然后在嗅灯泡中再生。 DDTC给药后3天的平均嗅鳞片重量在6周内逐渐恢复以控制值。嗅觉神经的DDTC诱导的病变导致谷胱甘肽（GSH）和嗅灯泡中的抗氧化酶活性的显着变化。相比之下，大脑或背侧Neocortex中没有发现显着的变化。这些观察结果表明，单剂量的DDTC选择性地影响了嗅灯泡的ROS清除系统。此外，这些变化持续至少6周，包括再生和突触突变。嗅鳞茎GSH浓度明显减少47 +/- 4％，谷胱甘肽还原酶活性减少18 +/- 3％，并在6周内增加27 +/- 7％。超氧化物歧化酶活性在病变后3天的大鼠嗅灯泡中显着降低32 +/- 6％，然后在3周内回收并增加38 +/- 3％。在整个病变后生存期内血液泡丙醛浓度（298 +/- 67％）升高（298 +/- 67％），尽管这种变化没有达到本研究所需的严格统计显着性水平。这些数据表明，在嗅觉神经再生过程中增加了ROS助熔剂渗透嗅灯泡抗氧化防御系统。

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