1,4-Dioxane (DXN) is used as solvent in different consumer products including cosmetics, paints, surfactants, and waxes. In addition, DXN is released as an unwanted contaminating by-product as a result of some reactions including ethoxylation of alcohols, which occurs with in personal care products. Consequently, DXN pollution was detected in drinking water and is considered as an environmental problem. At present, the genotoxicity effects attributed to DXN are controversial. The present study using an model organism aimed to determine the toxic/genotoxic, mutagenic/recombinogenic, oxidative damage as evidenced by ROS production, phenotypic alterations as well as behavioral and developmental alterations that are closely related to neuronal functions. Data demonstrated that nontoxic DXN concentration (0.1, 0.25, 0.5, or 1%) induced mutagenic (1%) and recombinogenic (0.1, 0.25, or 0.5%) effects in wing spot test and genotoxicity in hemocytes using comet assay. The nontoxic concentrations of DXN (0.1, 0.25, 0.5, or 1%) significantly increased oxidative stress, climbing behavior, thermal sensivity and abnormal phenotypic alterations. Our findings show that in contrast to exposure, DXN using an model this compound exerts toxic and genotoxic effects. Data suggest that additional studies using other models are thus warranted.
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http://dx.doi.org/10.1080/15287394.2022.2027832 | DOI Listing |
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