Acetaminophen exposure alters the DNA methylation pattern of Mugilogobius chulae, along with the changes in the Nrf2-Keap1 signaling pathway.

DNA methylation can dynamically regulate multiple physiological processes in organisms in response to changes of the external environment. The effects of acetaminophen (APAP) on DNA methylation in aquatic organisms and its toxic mechanisms is an interesting issue. In the present study, Mugilogobius chulae (Approximately 225 individual), a small benthic native fish, were employed to assess the toxic effects of APAP-exposure on non-target organisms.

Assessment of ecotoxicity effects of aspirin on non-target organism (Daphnia magna) via analysis of the responses of oxidative stress, DNA methylation-related genes expressions and life traits changes.

Aspirin (acetylsalicylic acid, ASA), a widely used non-steroidal anti-inflammatory drug, was frequently detected in aquatic environments around the world. However, information on the potential toxic effects of aspirin on non-target aquatic invertebrates is limited. In the present study, we investigated the effects of ASA on the transcriptional expressions of antioxidant genes (Nrf2, Keap1, HO-1, GCLC, GPx, TRX, TrxR and Prx1) and DNA methylation genes (DNMT1, DNMT3 and TET2) in Daphnia magna (D.

Hypoxia aggravates the burden of yellowstripe goby (Mugilogobius chulae) under atorvastatin exposure.

In the present study, an estuarine benthic fish, Mugilogobius chulae (M. chulae), was exposed to hypoxia, atorvastatin (ATV), a highly used and widely detected lipid-lowering drug in aquatic environment, and the combination of hypoxia and ATV for 7 days, respectively, so as to address and compare the effects of the combination of hypoxia and ATV exposure on M. chulae.

Response of the Sirtuin/PXR signaling pathway in Mugilogobius chulae exposed to environmentally relevant concentration Paracetamol.

Paracetamol (APAP) is one of the most widely used non-steroidal anti-inflammatory drugs, which is frequently detected in various water bodies. Studies are limited about its toxic effects and mechanisms on non-target aquatic organisms. In this study, an estuarine bottom-dwelling fish named Mugilogobius chulae, distributed in southern China, was selected as experimental species and the changes of PXR signaling pathway, a key signaling pathway of detoxification metabolic system in liver, were investigated under APAP exposure (0.

Simvastatin affects the PPARα signaling pathway and causes oxidative stress and embryonic development interference in Mugilogobius abei.

Simvastatin (SV) is a common hypolipidemic drug in clinical medicine that can reduce endogenous cholesterol biosynthesis by inhibiting hydroxyl-methyl-glutaryl coenzyme A reductase. SV took a large market share in the lipid-lowering drugs and it is frequently detected in various water bodies due to its increasing consumption in past years. In the present investigation, we selected a native fish species in the Pearl River Basin in China, Mugilogobius abei (M.

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.