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裂缝可卡因引起的遗传毒性、氧化应激和炎症反应与致癌作用的关系。

Genotoxicity, oxidative stress, and inflammatory response induced by crack-cocaine: relevance to carcinogenesis.

机构信息

Department of Biosciences, Federal University of São Paulo, UNIFESP, Rua Silva Jardim, 136, Room 332, Vila Mathias, Santos, SP, 11050-020, Brazil.

Department of Marine Sciences, Federal University of São Paulo, UNIFESP, Santos, SP, Brazil.

出版信息

Environ Sci Pollut Res Int. 2021 Mar;28(12):14285-14292. doi: 10.1007/s11356-021-12617-2. Epub 2021 Feb 3.

Abstract

Crack-cocaine is a cocaine by-product widely consumed by general population in developing countries. The drug is low cost and is associated with more intense effects when compared to other illicit drugs. Genotoxicity, oxidative stress, and inflammatory response are considered crucial events in carcinogenesis, since they actively participate in the multistep process. The purpose of this paper was to provide a mini review regarding the relationship between carcinogenesis and genotoxicity, oxidative stress, and inflammation induced by crack-cocaine. The present study was conducted on search of the scientific literature from the published studies available in PubMed, MEDLINE, Scopus, and Google Scholar for all kind of articles (all publications to November 2020) using the following key words: crack-cocaine, DNA damage, genotoxicity, cellular death, cytotoxicity, mutation, oxidative stress, inflammation, and mutagenicity. The results showed that published papers available were almost all in vivo test system being conducted in humans or rodents. Crack-cocaine was able to induce genotoxicity and oxidative stress in mammalian cells. However, the role of inflammatory response after exposure to crack-cocaine was not conclusive so far. In summary, this study is consistent with the notion that crack-cocaine is a chemical carcinogen as a result of genotoxicity and oxidative stress induced in mammalian and non-mammalian cells.

摘要

快克可卡因是一种由发展中国家普通人群广泛消费的可卡因副产品。与其他非法药物相比,该毒品价格低廉,且效果更强烈。遗传毒性、氧化应激和炎症反应被认为是致癌作用中的关键事件,因为它们积极参与多步骤过程。本文旨在提供关于快克可卡因引起的致癌作用与遗传毒性、氧化应激和炎症之间关系的简要综述。本研究在 PubMed、MEDLINE、Scopus 和 Google Scholar 上搜索了从已发表的研究中获得的科学文献,使用了以下关键词:快克可卡因、DNA 损伤、遗传毒性、细胞死亡、细胞毒性、突变、氧化应激、炎症和致突变性,以寻找各种文章(截至 2020 年 11 月的所有出版物)。结果表明,现有的已发表论文几乎都是在人类或啮齿动物中进行的体内测试系统。快克可卡因能够诱导哺乳动物细胞的遗传毒性和氧化应激。然而,迄今为止,接触快克可卡因后炎症反应的作用还没有定论。总之,这项研究与快克可卡因是一种化学致癌物的观点一致,因为它在哺乳动物和非哺乳动物细胞中引起遗传毒性和氧化应激。

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