Immune, inflammatory, autophagic and DNA damage responses to long-term H2O2 exposure in different tissues of common carp (Cyprinus carpio)

Hydrogen peroxide (H2O2) is a stable reactive oxygen species (ROS) in aquatic environment, and high concentration of ambient H2O2 may directly or indirectly affect aquatic animal health. However, the response mechanism of fish to ambient H2O2 has not been well studied yet. Therefore, the aim of the study was to investigate the immune, inflammatory, autophagic and DNA damage responses to long-term H2O2 exposure in different tissues of common carp. The results showed that H2O2 exposure induced a significant immune response, with alterations in the levels of immune parameters including AKP, ACP, LZM, C3, HSP90 and HSP70 in different tissues. The inflammatory response evoked by H2O2 exposure was associated with the activations of TLRs and NF-kappa B (P65) in the majority of tested tissues. The autophagy process was significantly affected by H2O2 exposure, evidenced by the upregulations of the autophagy-related genes in liver, gills, muscle, intestines, heart and spleen and the downregulations in kidney. Meanwhile, the mRNA level of atm, a primary transducer of DNA damage response, was upregulated in liver, gills, intestines and spleen, and the DNA damage was evidenced by increased 8-OHdG level in intestines after H2O2 exposure. Moreover, cell cycle regulation-related genes, including cyclin A1, B and/or E1, highly expressed in all tested tissues except heart after H2O2 exposure. Interestingly, IBR analysis exhibited that immune, inflammatory, autophagic and DNA damage responses to H2O2 exposure were in a dose-dependent and tissue-specific manner. These data may contribute to understanding H2O2 toxicity for fish and assessing potential risk of H2O2 in aquatic environment. (C) 2020 Elsevier B.V. All rights reserved.

Automated summary

The study investigated the responses of common carp to long-term H2O2 exposure, revealing significant immune, inflammatory, autophagic, and DNA damage responses in different tissues. The immune response was evident through changes in immune parameters, while the inflammatory response was associated with TLRs and NF-kappa B activation. Autophagy process and DNA damage response were affected by H2O2 exposure in a tissue-specific manner, with cell cycle regulation genes showing differential expression patterns. Overall, the responses to H2O2 exposure were dose-dependent and tissue-specific, providing insights into the potential toxicity and risk assessment of H2O2 in aquatic environments.