曲马多通过氧化应激诱导器官毒性的研究综述

IF 0.3 Q4 MEDICINE, LEGAL
L. Mohammadnejad, K. Soltaninejad
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引用次数: 2

摘要

背景:曲马多(TR)是一种合成的阿片类中枢镇痛药,用于各种疾病的中重度疼痛管理。大量研究支持曲马多的使用与氧自由基水平升高之间的联系。大量生产活性氧会产生二次毒性化合物。这可能会破坏细胞的内部成分,最终导致器官损伤。曲马多滥用的趋势越来越大,因该药物而中毒、滥用和死亡的报告也越来越多。因此,本研究旨在回顾急性和慢性接触曲马多通过氧化应激诱导器官毒性的动物和人类研究。方法:检索Pubmed、Google Scholar和Scopus文献数据库中研究氧化应激作为曲马多毒性机制的研究。对检索到的文章的参考文献列表进行了手动搜索。数据收集于2000年至2021年(截至2021年6月)。结果:从28篇关于TR诱导的氧化应激器官损伤的实验和人类研究的文章中,包括本综述中脂质过氧化的发生、总抗氧化能力水平的改变以及许多器官(如脑、肝、肾、,肾上腺和肺在曲马多暴露的实验研究中都有观察。结论:氧化应激可能是TR诱导组织损伤的最关键的毒性机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tramadol-Induced Organ Toxicity via Oxidative Stress : A Review Study
Background: Tramadol (TR) is a synthetic opioid-like centrally acting analgesic used for moderate to severe pain management in various diseases. Numerous investigations have supported the association between tramadol use and increased levels of oxygen-free radicals. Mass production of reactive oxygen species produces secondary toxic compounds. This could damage the internal components of the cell and ultimately causes organ damage. There exists a growing trend of tramadol abuse and the increasing reports of poisoning, abuse, and mortality due to this drug. Thus, the present study aimed to review the animals and human studies on the effects of acute and chronic exposure of tramadol in inducing organ toxicities through oxidative stress. Methods: Pubmed, Google Scholar, and Scopus bibliographic databases were searched for studies that investigated oxidative stress as a mechanism of toxicity by tramadol. A manual search of reference lists of the retrieved articles was conducted. Data were collected from 2000 to 2021 (up to June 2021). Results: From 28 articles concerning experimental and human studies of TR-induced oxidative stress organ damage, which included in this review, the occurrence of lipid peroxidation, alteration in the levels of total antioxidant capacity, and other oxidative stress biomarkers in many organs such as the brain, liver, kidney, adrenal and lung in the experimental studies of tramadol exposure have been observed. Conclusion: Oxidative stress could be considered the most critical toxic mechanism in TR-induced tissue damage.
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来源期刊
CiteScore
0.60
自引率
0.00%
发文量
50
审稿时长
12 weeks
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