# Melatonin Rescues Triclosan-Disrupted Porcine Oocyte Meiosis via Suppression of p53-Mediated Apoptosis

## TL;DR

Melatonin can protect pig oocytes from triclosan's harmful effects by preventing cell death and restoring normal development.

## Contribution

Melatonin's ability to rescue triclosan-impaired oocyte meiosis via p53-mediated anti-apoptotic effects is newly demonstrated.

## Key findings

- Triclosan disrupts porcine oocyte meiosis and induces apoptosis.
- Melatonin reverses triclosan-induced damage by suppressing the p53 pathway.
- Melatonin restores meiotic progression and proteomic balance in oocytes.

## Abstract

Triclosan (TCS), a widely used antimicrobial agent present in numerous consumer products such as soaps and toothpaste, has raised growing concerns regarding its potential adverse effects on fertility. In this study, we employed porcine oocytes as a model to investigate how TCS affects their development and whether melatonin, a natural hormone, can offer protection. We found that TCS exposure severely disrupts oocyte meiotic maturation and furthermore triggers apoptosis. Importantly, we discovered that melatonin effectively reverses this damage by suppressing the p53 pathway, an intrinsic stress-response system that would otherwise signal the oocytes to arrest their development and undergo programmed cell death. Our findings elucidate a mechanism through which melatonin protects oocyte quality and suggest its potential as a protective agent against the detrimental effects of common environmental chemicals on female fertility.

Triclosan (TCS), a widely used environmental antimicrobial agent, poses potential risks to female reproductive health, yet its toxic effects on oocyte maturation remain inadequately characterized. In this study, we established an in vitro maturation (IVM) model of porcine oocytes to investigate TCS-induced meiotic impairment and to evaluate the rescuing effects of melatonin (MT), an endogenous indoleamine with potent antioxidant and anti-apoptotic activities. Our results demonstrated that TCS exposure significantly disrupted oocyte maturation, as evidenced by suppressed polar body extrusion and compromised cumulus expansion. Furthermore, TCS triggered early apoptosis. Proteomic analysis revealed that the p53 signaling pathway was significantly dysregulated by TCS exposure. Notably, co-treatment with MT during IVM effectively restored meiotic progression, attenuated apoptosis, and rebalanced the disrupted proteomic profile. Mechanistic investigation, validated by Western blotting, confirmed that TCS upregulated p53 and downregulated its downstream cell cycle effector CCNB1 while concurrently altering the ratio of apoptosis-related proteins BAX/BCL-2. Melatonin treatment effectively normalized the expression of these key proteins (p53, CCNB1, BAX, and BCL-2). These findings illustrate that MT rescues TCS-impaired oocyte quality through p53-dependent suppression of apoptosis and restoration of meiotic progression, providing new insights into potential strategies for mitigating environmental pollutant-induced reproductive damage.