PDF(Pubmed)
Abstract：
The explosive compound 2,4,6-trinitrotoluene (TNT) is well known as a major component of munitions. In addition to its potential carcinogenicity and mutagenicity in humans, recent reports have highlighted TNT toxicities in diverse organisms due to its occurrence in the environment. These toxic effects have been linked to the intracellular metabolism of TNT, which is generally characterised by redox cycling and the generation of noxious reactive molecules. The reactive intermediates formed, such as nitroso and hydroxylamine compounds, also interact with oxygen molecules and cellular components to cause macromolecular damage and oxidative stress. The current review aims to highlight the crucial role of TNT metabolism in mediating TNT toxicity, via increased generation of reactive oxygen species. Cellular proliferation of reactive species results in depletion of cellular antioxidant enzymes, DNA and protein adduct formation, and oxidative stress. While TNT toxicity is well known, its ability to induce oxidative stress, resulting from its reductive activation, suggests that some of its toxic effects may be caused by its reactive metabolites. Hence, further research on TNT metabolism is imperative to elucidate TNT-induced toxicities.
摘要：
爆炸化合物2,4,6-三硝基甲苯（TNT）是众所周知的弹药的主要组成部分。除了它对人类的潜在致癌性和致突变性，最近的报道强调了TNT在不同生物中的毒性，因为它在环境中的发生。这些毒性作用与TNT的细胞内代谢有关，其特征通常是氧化还原循环和有害反应分子的产生。形成的反应中间体，如亚硝基和羟胺化合物，还与氧分子和细胞成分相互作用，导致大分子损伤和氧化应激。本综述旨在强调TNT代谢在介导TNT毒性中的关键作用。通过增加活性氧的产生。反应性物种的细胞增殖导致细胞抗氧化酶的消耗，DNA和蛋白质加合物的形成，和氧化应激。虽然TNT的毒性是众所周知的，它诱导氧化应激的能力，由于其还原活化，表明其某些毒性作用可能是由其反应性代谢物引起的。因此，对TNT代谢的进一步研究对于阐明TNT诱导的毒性至关重要。
