201 / 2024-09-11 12:02:59

Molecular Events in Response to Triclosan-Induced Oxidative Stress in CRISPR/Cas9-Mediated p53-Targeted Mutants in Daphnia magna

p53 gene,water flea,CRISPR/Cas9,triclosan,apoptosis

Triclosan, a widely used antimicrobial agent, has been implicated in oxidative stress induction and disruption of cellular processes in aquatic organisms. As triclosan is ubiquitous in the aquatic environment, many previous studies have documented the effects of triclosan exposure on aquatic organisms. Nevertheless, most of the research has concentrated on the molecular and physiological responses of triclosan but there are still limited studies on the function of specific genes and the consequences of their absence. In this study, we focused on p53, a gene that is crucial for molecular responses such as autophagy and apoptosis as a result of triclosan exposure. In order to ascertain the role and impact of the p53 gene in triclosan-induced molecular responses, we examined the molecular responses to triclosan-induced oxidative stress in wild-type (WT) and CRISPR/Cas9-mediated p53 mutant (MT) water fleas. The result has been accomplished by examining changes in molecular mechanisms, including in vivo endpoints, enzyme activities, ATP release rate, and apoptosis, to determine the role and impact of the p53 gene on triclosan-induced molecular responses. The results indicated that the sensitivity of MT water fleas to triclosan was greater than that of WT water fleas; however, the difference in sensitivity was significant at short exposures within 48 hours and decreased towards 48 hours. Accordingly, when we confirmed the oxidative stress after 24 hours of exposure, the oxidative stress to triclosan exposure was stronger in the MT group, with an imbalance of redox. To identify the mechanisms of tolerance to triclosan in WT and MT D. magna, we checked mitochondrial and ER-stress-related biomarkers and found an increase in apoptosis and greater sensitivity to triclosan exposure in the MT group than in WT. Our results suggest that the absence of p53 caused alterations in molecular processes in response to triclosan exposure, resulting in increased sensitivity to triclosan, and that p53 plays a critical role in response to triclosan exposure.