Emerging contaminants, such as the herbicides trifluralin and tebuthiuron, comprise a class of compounds for which toxicological data are lacking, especially data regarding their harmful effects and biomarkers of exposure. Their potential damage to the environment and non-target organisms makes understanding their toxic mechanisms an urgent matter. Mitochondria, which exert an energy production function, play a vital role in maintaining many cellular activities and therefore are reliable predictors of substance toxicity. This study evaluates whether the herbicides trifluralin and tebuthiuron (at concentrations ranging from 1 to 100 μM) affect isolated rat liver mitochondria. The herbicides were analyzed according to their ability to interact with the mitochondrial membrane and induce swelling, lipoperoxidation, ROS formation, and NAD(P)H oxidation; dissipate the membrane potential; dysregulate calcium homeostasis; and alter ATP and GSH/GSSG levels. Tebuthiuron does not disrupt the mitochondrial biochemistry at any of the tested concentrations. In contrast, trifluralin can disturb the mitochondrial respiration, especially at the highest concentration, but it cannot induce oxidative stress. These results suggest that the aforementioned effects can occur as toxic mechanisms of trifluralin in non-target organisms, as well.

中文翻译：

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氟乐灵和戊硫脲是否会损害离体的大鼠肝脏线粒体？

新出现的污染物，如除草剂氟乐灵和丁硫脲，包括一类缺乏毒理学数据的化合物，尤其是关于其有害影响和接触生物标志物的数据。它们对环境和非目标生物的潜在损害使得了解它们的毒性机制成为当务之急。线粒体发挥能量生产功能，在维持许多细胞活动中起着至关重要的作用，因此是物质毒性的可靠预测因子。本研究评估了除草剂氟乐灵和丁硫脲（浓度范围为 1 至 100 μM）是否影响分离的大鼠肝线粒体。根据除草剂与线粒体膜相互作用并诱导肿胀、脂质过氧化、ROS 形成和 NAD(P)H 氧化的能力进行分析；耗散膜电位；钙稳态失调；并改变 ATP 和 GSH/GSSG 水平。Tebuthiuron 在任何测试浓度下都不会破坏线粒体生物化学。相比之下，氟乐灵可以干扰线粒体呼吸，尤其是在最高浓度时，但不能诱导氧化应激。这些结果表明，上述作用也可以作为氟乐灵在非靶标生物中的毒性机制发生。