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亚慢性铅暴露改变大鼠脑组织氧化应激标志物、乙酰胆碱酯酶和 Na+/K+-ATP 酶活性。

Sub‑chronic administration of lead alters markers of oxidative stress, acetylcholinesterase and Na+K+‑ATPase activities in rat brain.

机构信息

Postgraduate Program in Health and Environment, Universidade da Região de Joinville (UNIVILLE), Joinville, SC, Brasil.

Department of Natural Science, Center for Exact and Natural Sciences, Universidade Regional de Blumenau, Blumenau, SC, Brasil.

出版信息

Acta Neurobiol Exp (Wars). 2023;83(2):216-225. doi: 10.55782/ane-2023-019.

Abstract

This study investigated the effects of sub‑chronic administration of lead (Pb) acetate on thiobarbituric acid reactive substances (TBA‑RS), total sulfhydryl content, protein carbonyl content, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH‑Px]), acetylcholinesterase (AChE), and Na+K+‑ATPase in the cerebral structures of rats. Male Wistar rats aged 60 days were treated with saline (control group) or Pb (treatment group), at various doses, by gavage, once a day for 35 days. The animals were sacrificed twelve hours after the last administration, and the cerebellum, hippocampus and cerebral cortex were removed. The results showed that Pb did not alter the evaluated oxidative stress parameters. Furthermore, Pb (64 and/or 128 mg/kg) altered SOD in the cerebellum, cerebral cortex and hippocampus. Pb (128 mg/kg) altered CAT in the cerebellum and cerebral cortex and GSH‑Px in the cerebral cortex. Also, Pb (64 mg/kg and 128 mg/kg) altered GSH‑Px in the cerebellum. Moreover, Pb (128 mg/kg) increased AChE in the hippocampus and decreased Na+K+‑ATPase in the cerebellum and hippocampus. In conclusion, sub‑chronic exposure to Pb (occupational and environmental intoxication) altered antioxidant enzymes, AChE, and Na+K+‑ATPase, contributing to cerebral dysfunction.

摘要

这项研究调查了亚慢性醋酸铅(Pb)给药对大鼠脑结构中硫代巴比妥酸反应物质(TBA-RS)、总巯基含量、蛋白羰基含量、抗氧化酶(超氧化物歧化酶[SOD]、过氧化氢酶[CAT]、谷胱甘肽过氧化物酶[GSH-Px])、乙酰胆碱酯酶(AChE)和 Na+K+-ATP 酶的影响。60 天大的雄性 Wistar 大鼠经灌胃给予生理盐水(对照组)或不同剂量的 Pb(治疗组),每天一次,共 35 天。动物在最后一次给药后 12 小时处死,取出小脑、海马和大脑皮质。结果表明,Pb 未改变评估的氧化应激参数。此外,Pb(64 和/或 128 mg/kg)改变了小脑、大脑皮质和海马中的 SOD。Pb(128 mg/kg)改变了小脑和大脑皮质中的 CAT 和大脑皮质中的 GSH-Px。此外,Pb(64 mg/kg 和 128 mg/kg)改变了小脑中的 GSH-Px。此外,Pb(128 mg/kg)增加了海马中的 AChE,降低了小脑和海马中的 Na+K+-ATP 酶。总之,亚慢性 Pb 暴露(职业和环境中毒)改变了抗氧化酶、AChE 和 Na+K+-ATP 酶,导致大脑功能障碍。

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