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Environ Toxicol Chem. 2016 Aug;35(8):2041-7. doi: 10.1002/etc.3349. Epub 2016 May 27.

Ecotoxicological evaluation of low-concentration bisphenol A exposure on the soil nematode Caenorhabditis elegans and intrinsic mechanisms of stress response in vivo.

Author information

1
State Environmental Protection Key Laboratory of Environmental Risk Assessment and Control on Chemical Process, State Key Laboratory of Bioreactor Engineering, School of Resources and Environmental Engineering, East China University of Science and Technology, Shanghai, People's Republic of China.
2
Research Institute of Wastes and Soil Remediation, Shanghai Academy of Environmental Sciences, Shanghai, People's Republic of China.

Abstract

As a representative species of nematodes, Caenorhabditis elegans is an attractive animal model for evaluating ecotoxicological effects and intrinsic mechanisms of the stress response in vivo. To acquire a better knowledge of environmental effects of bisphenol A (BPA), ecotoxicological evaluations were conducted using C. elegans on the physiological (growth, locomotion behaviors, and reproduction), biochemical (lipofuscin accumulation, reactive oxygen species production, and cell apoptosis), and molecular (stress-related gene expression) responses. Nematodes were exposed to BPA (0.001-10 µM) in 2 assay systems (L4 larvae for 24 h and L1 larvae for 72 h). Exposure to BPA could significantly (p < 0.05) alter body length, locomotion behaviors, brood size, cell apoptosis, and selected stress-related gene expression. At the physiological level, BPA exerted adverse effects on nematodes at the microgram per liter level in both assay systems, with head thrashes as the most sensitive endpoint. At the biochemical level, apoptosis degree showed increases at concentrations above 0.1 µM in both assay systems. At the molecular level, BPA induced increases in selected stress-related gene expression, even at the lowest tested concentration. In addition, BPA-induced cell apoptosis was suggested as a potential mode of action, resulting in adverse physiological effects. Therefore, BPA exposure was speculated to impose developmental, reproductive, and neurobehavioral toxicities on C. elegans and caused variations of stress-related gene expression. Environ Toxicol Chem 2016;35:2041-2047.

KEYWORDS:

Bisphenol A; Caenorhabditis elegans; Cell apoptosis; Multiple toxicological endpoints; Stress-related gene expression

PMID:
26748796
DOI:
10.1002/etc.3349
[Indexed for MEDLINE]

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