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Effect of Chronic Hydrogen Peroxide Exposure on Ion Transport in Gills of Common Carp (Cyprinus carpio)

Yating Mou; Bing Li; Yiran Hou; Rui Jia; Jian Zhu
Fishes · Vol. 8, Issue 3 · pp. 134 · 2023

Abstract

High environmental hydrogen peroxide (H2O2) has been demonstrated to be toxic for fish. However, the response mechanism of fish to chronic H2O2 exposure is not yet well understood. Therefore, this study aimed to investigate the alteration in ion transport in gills and analyzed the potential response mechanism after chronic H2O2 exposure. The common carps were exposed to 0, 0.25, 0.50, and 1.00 mM of H2O2 for 14 days. The histopathological evaluation results indicated that H2O2 exposure caused incomplete gill filament structure. In the plasma, H2O2 exposure suppressed the potassium (K+) concentration but increased sodium (Na+) concentration. In the gills, the calcium (Ca2+) level was raised, but the K+ and chlorine (Cl−) levels were decreased after H2O2 exposure. After 14 days of exposure, H2O2 prompted the activities of Ca2+/Mg2+-ATPase and H+/K+-ATPase but suppressed Na+/K+-ATPase activity in the gills. Gene transcription analysis showed that the ion-regulation-related genes including nkaa and rhbg were downregulated after H2O2 exposure. In addition, H2O2 exposure upregulated the mRNA levels of cam and camk II, indicating that the Ca2+ singling pathway was activated. In conclusion, our data showed that chronic H2O2 exposure altered gill structure and disturbed ion transport, which further negatively affected the equilibrium of ions and osmotic pressure.

Bibliographic Information

JournalFishes
PublisherMDPI
Publication Date2023-02-26
Publication Year2023
Volume8
Issue3
Pages134
Document TypeJournal Article
eISSN2410-3888
DOI10.3390/fishes8030134
SubjectFisheries; fish biology; aquaculture; aquatic ecology; fisheries management

Access Information

NARA Access CoverageOA / free full text
Journal Homepagehttps://www.mdpi.com/journal/fishes
Publisher PageOpen Publisher Page
This article is openly available from the publisher.