Atorvastatin causes oxidative stress and alteration of lipid metabolism in estuarine goby Mugilogobius abei.

The potential effects of the environmental residues of Atorvastatin (ATV) as a widely used antilipemic agent on aquatic organisms deserve more investigations because of its high detection frequency in environment. The responses of Nrf2/Keap1 signaling pathway (including the transcriptional expression of Nrf2, Keap1, GCLC, GPx, GST, SOD, CAT, Trx2, TrxR, HMG-CoAR and PGC-1α) in Mugilogobius abei were investigated under acute and sub-chronic exposure of ATV in the simulated laboratory conditions. The changes of related enzymatic activity (GST, GPx, SOD, CAT and TrxR) and the content of GSH and MDA combining with the observation of histology sections of liver in M. abei were also addressed. The results show Nrf2 and its downstream antioxidant genes were induced to different degrees under ATV exposure. The activities of antioxidant enzymes were inhibited at 24 h and 72 h but induced/recovered at 168 h. Correspondingly, negatively correlated to GSH, MDA increased first but reduced then. Notably, with the increase of exposure concentration/time, the volume of lipid cells in liver decreased, suggesting more lipid decomposition. Therefore, lipid metabolism was suppressed (down-regulation of PGC-1α) and cholesterol biosynthesis was induced (up-regulation of HMG-COAR) at 168 h. In short, ATV brings oxidative stress to M. abei in the initial phase. However, with the increase of exposure time, ATV activates Nrf2/Keap1 signaling pathway and improves the antioxidant capacity of M. abei to reverse this adverse effect. ATV also affects lipid metabolism of M. abei by reducing cholesterol content and accelerating lipid decomposition.