Cytotoxic effects of pentachlorophenol (PCP) and its metabolite tetrachlorohydroquinone (TCHQ) on liver cells are modulated by antioxidants |
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Authors: | Constanze Pietsch Juliane Hollender Falk Dorusch Patricia Burkhardt-Holm |
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Affiliation: | 1. Institute of Natural Resource Sciences (IUNR), Zurich University of Applied Sciences (ZHAW), Gruental, P.O. Box, 8820, Waedenswil, Switzerland 2. Man–Society–Environment, Department of Environmental Sciences, University Basel, Vesalgasse 1, 4051, Basel, Switzerland 3. Eawag, Swiss Federal Institute of Aquatic Science and Technology, überlandstrasse 133, 8600, Dübendorf, Switzerland 4. Department of Biological Sciences, University of Alberta, CW 405 Biological Sciences Building, Edmonton, AB, T6G 2E9, Canada
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Abstract: | The worldwide distribution and high bioaccumulation potential of pentachlorophenol (PCP) in aquatic organisms imply a high toxicological impact in aquatic systems. Firstly, our investigations show that, similar to mammalian cell lines, PCP can be metabolized to tetrachlorohydroquinone (TCHQ) in the permanent cell line derived from rainbow trout liver cells (RTL-W1). Moreover, we demonstrate that PCP as well as its metabolite TCHQ is capable of influencing the viability of these cells. Three cell viability assays were performed to assess possible cellular targets of these substances. Thus, the cytotoxicity of the PCP-derivative TCHQ was shown for the first time in a fish cell line. Further investigations revealed the involvement of ROS in the cytotoxicity of PCP and its metabolite TCHQ. The observation of oxidative stress provides a plausible explanation for the increased cytotoxicity at higher concentrations especially for PCP and implies possible mechanisms underlying these observations. In addition, antioxidants such as ascorbic acid and quercetin modulate the detrimental effects of PCP and TCHQ whereby both compounds exacerbate the cytotoxic effects of high PCP and TCHQ concentrations. |
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