Environmentally relevant concentrations of carbamazepine induced lipid metabolism disorder of Chinese rare minnow (Gobiocypris rarus) in a gender-specific pattern

Carbamazepine (CBZ), an anticonvulsant and mood stabilizer, is ubiquitous distributed in aquatic environment. Though the toxicity and endocrine disrupting effect of CBZ on non-target organisms have been studied, its lipotoxity are scarcely known. To assess the lipotoxicity of CBZ, 2-month-old Chinese rare minnow were exposed to 0, 1, 10, and 100 mu g/L CBZ for 90 d. Obvious dyslipidemia was observed after 30 d and 90 d exposure, whereas overt hyperlipidemia was observed in males at 100 mu g/L treatments. Severe lipid droplet accumulation in livers was observed at 10 and 100 mu g/L treatments for 30 d and in females, whereas those was observed at all treatments in males. In addition, serious mitochondria damage was observed in males at 100 mu g/L treatments. After 90 d exposure, the enzyme activities of FAS and ACCa were significantly increased at 10 and 100 mu g/L treatments, whereas HMGCR were markedly increased at 100 mu g/L treatments (p < 0.05). However, ACC beta were markedly decreased in females at 10 and 100 mu g/L treatments and in males at all treatments (p < 0.05). The transcription levels of fasn, acc alpha, hmgcr alpha, fdft1, idi1, plin1,plin2, caveolin1, and caveolin2 were significantly increased at 100 mu g/L treatments (p < 0.05). Moreover, the body weight was obviously increased at 10 and 100 mu g/L treatments in males (p < 0.05). Our results confirmed that environmental relevant concentrations CBZ induced lipid metabolism disorder and mitochondria damage of Chinese rare minnow in a gender-specific pattern, which provided a new insight into the lipotoxicity mechanism of CBZ. (C) 2020 Elsevier Ltd. All rights reserved.

Automated summary

This study found that exposure to CBZ induced lipid metabolism disorder and mitochondria damage in Chinese rare minnows, showing a gender-specific pattern. The results provide a new insight into the lipotoxicity mechanism of CBZ.