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논문 기본 정보

자료유형
학술저널
저자정보
Mohammad A. Alfhili (East Carolina University) 윤동석 (East Carolina Univ.) Taki A. Faten (East Carolina University) Jocelyn A. Francis (East Carolina University) 차동석 (우석대학교) Baohong Zhang (East Carolina University) Xiaoping Pan (East Carolina University) 이면희 (East Carolina University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제41권 제12호
발행연도
2018.12
수록면
1,052 - 1,060 (9page)
DOI
10.14348/molcells.2018.0378

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Triclosan (TCS) is a phenolic antimicrobial chemical used in consumer products and medical devices. Evidence from in vitro and in vivo animal studies has linked TCS to numerous health problems, including allergic, cardiovascular, and neurodegenerative disease. Using Caenorhabditis elegans as a model system, we here show that short-term TCS treatment (LC50: ~0.2 mM) significantly induced mortality in a dosedependent manner. Notably, TCS-induced mortality was dramatically suppressed by co-treatment with non-ionic surfactants (NISs: e.g., Tween 20, Tween 80, NP-40, and Triton X-100), but not with anionic surfactants (e.g., sodium dodecyl sulfate). To identify the range of compounds susceptible to NIS inhibition, other structurally related chemical compounds were also examined. Of the compounds tested, only the toxicity of phenolic compounds (bisphenol A and benzyl 4-hydroxybenzoic acid) was significantly abrogated by NISs. Mechanistic analyses using TCS revealed that NISs appear to interfere with TCS-mediated mortality by micellar solubilization. Once internalized, the TCS-micelle complex is inefficiently exported in worms lacking PMP-3 (encoding an ATP-binding cassette (ABC) transporter) ransmembrane protein, resulting in overt toxicity. Since many EDCs and surfactants are extensively used in commercial products, findings from this study provide valuable insights to devise safer pharmaceutical and nutritional preparations.

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