The increasing utilization of novel chemical substances and the repurposing of existing ones across diverse industries, including agriculture, cosmetics, food, and pharmaceuticals, underscores the imperative to assess potential environmental and human risks. Within these concerns, mitochondrial toxicity emerges as a notable challenge, often unintentionally resulting from drug interactions and leading to adverse health consequences. Mounting evidence indicates that mitochondrial dysfunction assumes a central role in various pathologies, such as metabolic disorders, accelerated aging, neurodegenerative diseases, and xenobiotic-induced organ toxicity. Notably, only in the past two decades has the concept of mitochondrial dysfunction as a direct toxic effect of drug exposure gained substantial consideration. Understanding mitochondrial dysfunction is pivotal for ensuring the safety of drugs and chemicals, unraveling disease mechanisms, and conducting risk assessments concerning different compounds and environmental factors. Our research focuses on elucidating cellular damage induced by chemicals in in vitro models, with a specific emphasis on mitochondria as a crucial target. This characterization is achieved through the utilization of mitochondrial-specific assays and transcriptomics, employing different models with distinct metabolic profiles that may exhibit varying susceptibilities to mitochondrial toxicity. This initiative highlights the importance of using appropriate cellular models, understanding cellular responses, and refining experimental parameters to achieve a deeper understanding of compound effects. Ultimately, these endeavors contribute to the development of more effective methods for toxicity assessment and the prompt identification of issues related to mitochondrial function.
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