揭示硫代乙酰胺诱导的毒性:多器官损伤和遗漏的骨毒性。

Haodong Zhang, Jian Xu
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摘要

硫代乙酰胺(TAA)是一种被广泛使用的肝毒性物质,在诱导肝衰竭疾病模型方面具有显著的优势。给实验动物施用 TAA 后,会产生强效氧化衍生物,最终激活氧化应激,并通过血液传播对多个器官造成严重损害。本综述总结了以往在毒理学动物实验中使用 TAA 的研究中观察到的各种器官损伤和相应的机理解释。暴露于 TAA 引起的主要病理后果包括氧化应激、炎症、脂质过氧化、纤维化、细胞凋亡诱导、DNA 损伤和破骨细胞形成。最近关于 TAA 骨毒性的体内和体外研究证实,长期大剂量使用 TAA 不仅会诱发实验动物的肝损伤,还会伴随骨损伤,而这一点长期以来一直被忽视。利用 TAA 建立实验动物疾病模型,通过控制 TAA 剂量、使用时间和动物暴露环境,可以诱导多种器官损伤模型。值得注意的是,TAA 诱导的损伤具有时间依赖性。最后,在日常生活中,尤其是对于研究人员来说,我们应该采取预防措施,尽量减少 TAA 暴露,降低相关器官损伤的概率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unveiling thioacetamide-induced toxicity: Multi-organ damage and omitted bone toxicity.

Thioacetamide (TAA), a widely employed hepatotoxic substance, has gained significant traction in the induction of liver failure disease models. Upon administration of TAA to experimental animals, the production of potent oxidative derivatives ensues, culminating in the activation of oxidative stress and subsequent infliction of severe damage upon multiple organs via dissemination through the bloodstream. This review summarized the various organ damages and corresponding mechanistic explanations observed in previous studies using TAA in toxicological animal experiments. The principal pathological consequences arising from TAA exposure encompass oxidative stress, inflammation, lipid peroxidation, fibrosis, apoptosis induction, DNA damage, and osteoclast formation. Recent in vivo and in vitro studies on TAA bone toxicity have confirmed that long-term high-dose use of TAA not only induces liver damage in experimental animals but also accompanies bone damage, which was neglected for a long time. By using TAA to model diseases in experimental animals and controlling TAA dosage, duration of use, and animal exposure environment, we can induce various organ injury models. It should be noted that TAA-induced injuries have a time-dependent effect. Finally, in our daily lives, especially for researchers, we should take precautions to minimize TAA exposure and reduce the probability of related organ injuries.

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