Do trifluralin and tebuthiuron impair isolated rat liver mitochondria?

Abstract

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.