Avaliação da biossegurança de novas moléculas calcogênias em Caenorhabditis elegans

Abstract

This study evaluated the biosafety and toxicological effects of AZT chalcogen derivatives (zidovudine), focusing on reducing mitochondrial toxicity, using the nematode Caenorhabditis elegans as an experimental model. Structural modifications to AZT, such as the ingestion of selenium and sulfur atoms, were explored to minimize the adverse effects associated with prolonged use of the drug, preserving its therapeutic efficacy. The results indicated that AZT induces significant mitochondrial dysfunction, including reduced membrane potential, decreased ATP levels, and changes in oxygen consumption. However, compromises such as ASAT-4-Cl and 7D received lower toxicity, better preserving cellular bioenergetics and causing less impact on behavioral parameters such as pharyngeal bombardment and locomotion. These compounds were promising in the development of safer and more effective therapeutic alternatives. The findings reinforce the potential of C. elegans as a model for toxicology and pharmacology studies, contributing to advances in the design of new AZT analogues with lower mitochondrial toxicity and greater safety for clinical applications.