ArticleAnimals : an open access journal from MDPI2025
Triclosan Caused Oocyte Meiotic Arrest by Modulating Oxidative Stress, Organelle Dysfunctions, Autophagy, and Apoptosis in Pigs.
Article in Animals : an open access journal from MDPI, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Sublethal Triclosan triggers oxidative stress and autophagy responses in Labeo rohita.Fish physiology and biochemistry · 2026Article
- Melatonin Rescues Triclosan-Disrupted Porcine Oocyte Meiosis via Suppression of p53-Mediated Apoptosis.Animals : an open access journal from MDPI · 2025Article
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
- Oocyte Exposure to Low Levels of Triclosan Has a Significant Impact on Subsequent Embryo Physiology.International journal of environmental research and public health · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Triclosan (TCS) is a highly effective broad-spectrum antibacterial agent; however, the specific roles of TCS in oocyte maturation remain poorly understood. This research investigated the influence of TCS on biologically active processes during the in vitro maturation of porcine oocytes. Our results demonstrated that TCS significantly decreased the maturation rate of porcine oocytes in a concentration-dependent manner and impaired cumulus expansion. These detrimental effects were mediated by the disruption of mitochondrial function and distribution, leading to oxidative stress characterized by an accumulation of reactive oxygen species (ROS), a decrease in the expression of the antioxidant enzymes SOD2 and GSH, reduced ATP production, and a loss of mitochondrial membrane potential (ΔΨm). We also observed interference with endoplasmic reticulum (ER) distribution, disturbances in Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.