Effects of glutaraldehyde and povidone-iodine on apoptosis of grass carp liver and hepatocytes.

Since disinfectants are used all over the world to treat illnesses in people and other animals, they pose a major risk to human health. The comprehensive effects of disinfectant treatments on fish liver, especially the impacts on oxidative stress, toxicological effects, transcriptome profiles, and apoptosis, have not yet been fully analyzed. In the current investigation, healthy grass carp were exposed to 80 µg/L glutaraldehyde or 50 µg/L povidone-iodine for 30 days. First, the findings of enzyme activity tests demonstrated that the administration of glutaraldehyde could considerably increase oxidative stress by lowering T-SOD, CAT, and GPx and raising MDA. Furthermore, KEGG research revealed that exposure to glutaraldehyde and povidone-iodine stimulated the PPAR signal pathway. To further elucidate the transcriptome results, the relative expressions of related DEGs in the PPAR signal pathway were verified. Glutaraldehyde induced apoptosis in liver tissue of grass carp; however, it activated cytotoxicity and apoptosis in grass carp hepatocytes when exposed to glutaraldehyde or povidone-iodine. According to the current study, disinfectants can cause the impairment of the immune system, oxidative stress, and attenuation of the PPAR signal pathway in the liver of grass carp, making them detrimental as dietary supplements for grass carp, particularly in the aquaculture sector.

Hemoglobin induces inflammation through NF-kB signaling pathway and causes cell oxidative damage in grass carp (Ctenopharyngodon idella).

Hemolytic disease in grass carp (C. idella) leads to hemolysis in vivo, releasing damage-related molecular patterns (DAMPs) hemoglobin (Hb; which is rapidly oxidized to Hb-Fe3+ and Hb-Fe4+) and generating a high level of reactive oxygen species (ROS) that cause oxidative damage. However, the effect of cell-free Hb on tissue cells of grass carp has yet to be elucidated. In this study, western blotting (WB) and immunofluorescence analysis (IFA) results showed that PHZ-induced hemolysis caused Hb and iron accumulation, increased the production of ROS and resulted in apoptosis in head kidney and middle kidney of the grass carp. Quantitative real-time PCR (qRT-PCR), WB, and IFA revealed that PHZ-induced hemolysis significantly upregulated the expression of inflammation-related genes through activation of the NF-κB signaling pathway. To further explore the effect of Hb, three forms of Hb (Hb, MetHb, and FerrylHb) were prepared. The incubation with the different forms of Hb and heme markedly upregulated the expression of cytokine genes through NF-κB signaling pathway, which was further confirmed by a specific inhibitor (caffeic acid phenethyl ester, CAPE). Flow cytometry analysis data showed that the stimulation of different forms of Hb and heme increased the production of ROS, and resulted in apoptosis. In summary, our data suggest that the excess cell-free Hb released during hemolysis modulates the inflammatory response through activation of the NF-κB signaling pathway and causes cell oxidative damage and apoptosis.