Effects of antibiotics on immunity and apoptosis on grass carp liver and hepatocytes

Abstract

Antibiotics are used to treat illnesses in animals and humans worldwide. Yet, many antibiotics and other secondary metabolites can contaminate the water supply, creating a substantial risk to human health. A comprehensive investigation is currently focusing on the systematic effects of dietary antibiotics on fish liver, particularly on their impacts on oxidative stress, transcriptome profiles, toxicity, and apoptosis. In the present study, healthy grass carp were treated orally with 10 mg/kg enrofloxacin or florfenicol for 14 days. The enzyme activity outcomes reflected that the administration of enrofloxacin or florfenicol could significantly induce oxidative stress by decreasing CAT, SOD and GPx and increasing MDA. In addition, KEGG analysis showed that both antibiotics activated the PPAR signal pathway. The expression levels of the six genes, namely FABP6, APOA1, CYP27A1, ACSL1, CPT1A, and ANGPTL4, in the PPAR signal pathway were determined to further clarify the transcriptomic data. Enrofloxacin induced apoptosis in grass carp liver tissue, while hepatocytes from grass carp treated with enrofloxacin and florfenicol activated cytotoxicity and apoptosis. The present study suggests that antibiotics can induce antioxidant stress, impair the immune system, and attenuate the PPAR signal pathway in the grass carp liver, thus being harmful to grass carp as a dietary supplement, mainly within the aquaculture industry.