Marine fatty acids aggravate hepatotoxicity of α-HBCD in juvenile female BALB/c mice |
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Affiliation: | 1. Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, No. 457 Zhongshan Road, Dalian 116023, China;2. University of Chinese Academy of Sciences, Beijing 100049, China;1. Center for Environmental Health Sciences, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan;2. Graduate School of Engineering, Kyoto University, Kyoto daigaku-Katsura, Nishikyo-ku, Kyoto 615-8530, Japan;1. URAFPA, Université de Lorraine, INRA USC340, Vandoeuvre les Nancy, France;2. LUNAM Université, Oniris, LABERCA, INRA USC1329, Nantes, France;3. ITAVI, Centre INRA de Tours, Nouzilly, France |
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Abstract: | Oily fish, a source of long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFAs), may contain persistent organic pollutants (POPs), including α-hexabromocyclododecane (α-HBCD). In experimental studies, marine LC n-3 PUFAs ameliorate fatty liver development while HBCD exposure was found to cause liver fatty acid (FA) changes. The present study investigated interactions of FAs and α-HBCD in juvenile female BALB/c mice using a factorial design. Mice (n = 48) were exposed for 28 days to a low (100 μg*kg body weight (BW)−1*day−1) or high dose (100 mg*kg BW−1*day−1) of α-HBCD in diets with or without LC n-3 PUFAs. High dose α-HBCD affected whole body lipid metabolism leading to changes in body weight and composition, and pathological changes in hepatic histology, which surprisingly were aggravated by dietary LC n-3 PUFAs. Hepatic FA profiling and gene expression analysis indicated that the dietary modulation of the hepatotoxic response to the high dose of α-HBCD was associated with differential effects on FA β-oxidation. Our results suggest that in a juvenile mouse model, marine FAs accentuate hepatotoxic effects of high dose α-HBCD. This highlights that the background diet is a critical variable in the risk assessment of POPs and warrants further investigation of dietary mediated toxicity of food contaminants. |
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Keywords: | Hexabromocyclododecane Nutritional modulation Juvenile toxicity Marine fatty acids |
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