Efeitos tóxicos do reteno em Caenorhabditis elegans: indução de estresse oxidativo, disfunção mitocondrial e neurodegeneração

Abstract

This study systematically investigated the toxic effects of retene, a non-priority polycyclic aromatic hydrocarbon (PAH), using Caenorhabditis elegans as an experimental model. PAHs are organic compounds widely distributed in the environment, primarily generated by the incomplete combustion of organic matter and fossil fuels. As persistent pollutants, they are associated with soil, water, and air contamination, posing a significant public health and environmental problem due to their carcinogenic, mutagenic, and toxic potential to various organisms. Exposure to retene compromised multiple physiological and cellular aspects of the organism, including egg hatching rate, motility, production of reactive oxygen species (ROS), lifespan, apoptosis in germ cells, mitochondrial dynamics, and integrity of dopaminergic neurons. Although egg laying and body growth were not significantly affected, there was a reduction in hatching at the end of the reproductive period, suggesting late embryonic effects. A significant reduction in body bends at higher doses was also observed, indicating possible neuromotor impairment. Retene exposure increased ROS production and triggered apoptosis in germ cells, in addition to altering mitochondrial morphology and increasing mitochondrial mass, especially at higher concentrations, possibly due to impaired mitophagy. Regarding lifespan, results revealed a non-linear response, with a significant increase in mean lifespan at the extreme concentrations (1 and 50 μg/mL), suggesting a possible hormetic effect. Additionally, retene induced progressive, dose-dependent dopaminergic neurodegeneration, with more pronounced effects in the early stages of exposure. These findings reinforce the toxic potential of retene even though it is not on the priority PAH list and demonstrate the applicability of C. elegans as an effective model for environmental toxicological assessments. The results contribute to understanding the mechanisms involved in retene toxicity, highlighting the central role of oxidative stress, mitochondrial dysfunction, and neurodegeneration.