Toxic Effects of Bisphenol A, Propyl Paraben, and Triclosan on Caenorhabditis elegans

International Journal of Environmental Research and Public Health

Lesly Patricia Tejeda-Benítez¹  María Cecilia García-Espiñeira²  Jesus Olivero-Verbel² 

[1] Biological, Toxicological and Environmental Sciences Research Group, School of Medicine, University of Cartagena, Zaragocilla Campus, Cartagena 130015, Colombia;Environmental and Computational Chemistry Group, School of Pharmaceutical Sciences, University of Cartagena, Zaragocilla Campus, Cartagena 130015, Colombia;

关键词: emerging contaminants;    Bisphenol A;    propyl paraben;    triclosan;    Caenorhabditis elegans;   

DOI  :  10.3390/ijerph15040684

来源: DOAJ

【 摘 要 】

Bisphenol A (BPA) is a ubiquitous plasticizer which is absorbed by ingestion and dermal contact; propyl paraben (PPB) inhibits the microbiome and extends the shelf life of many personal care products, whereas triclosan (TCS) is commonly found in antiseptics, disinfectants, or additives. In this work, Caenorhabditis elegans was used as a biological model to assess the toxic effects of BPA, PPB, and TCS. The wild type strain, Bristol N2, was used in bioassays with the endpoints of lethality, growth, and reproduction; green fluorescent protein (GFP) transgenic strains with the hsp-3, hsp-4, hsp-16.2, hsp-70, sod-1, sod-4, cyp-35A4, cyp-29A2, and skn-1 genes were evaluated for their mRNA expression through fluorescence measurement; and quick Oil Red O (q ORO) was utilized to stain lipid deposits. Lethality was concentration-dependent, while TCS and PPB showed more toxicity than BPA. BPA augmented worm length, while PPB reduced it. All toxicants moderately increased the width and the width–length ratio. BPA and PPB promoted reproduction, in contrast to TCS, which diminished it. All toxicants affected the mRNA expression of genes related to cellular stress, control of reactive oxygen species, and nuclear receptor activation. Lipid accumulation occurred in exposed worms. In conclusion, BPA, PPB, and TCS alter the physiology of growth, lipid accumulation, and reproduction in C. elegans, most likely through oxidative stress mechanisms.

【 授权许可】

Unknown