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H 2 S‐tolerant Fish Differentially Express Genes and Modify Mitochondrial Function to Maintain H 2 S Homeostasis
Author(s) -
Shaw Jennifer,
Henpita Chathurika,
Tobler Michael
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.640.3
Subject(s) - homeostasis , biology , mitochondrion , microbiology and biotechnology , function (biology) , hydrogen sulfide , zebrafish , oxidative phosphorylation , gene , chemistry , genetics , biochemistry , sulfur , organic chemistry
Hydrogen sulfide (H 2 S) is a toxic gas that inhibits the final step in the mitochondrial electron transport chain. This gas, however, is produced endogenously at low levels to promote vasodilation, angiogenesis, and reduce inflammation. Both a deficiency and an excess of H 2 S are associated with disease therefore, maintaining H 2 S homeostasis is critical for proper physiologic function. Despite the surge in biomedical interest in H 2 S as a therapeutic and a factor in the etiology of disease, the regulatory mechanisms remain largely unknown. Progress has been hampered by the lack of study systems that exhibit both sulfide susceptibility and sulfide tolerance within a single species that would permit comparative analyses toward uncovering mechanisms that regulate responses to H 2 S. Poecilia mexicana is a species of fish with populations that are naturally adapted to either non‐sulfidic or sulfidic environments. Offspring reared in the lab under non‐sulfidic conditions maintain their tolerance or non‐tolerance to H 2 S. We hypothesized that H 2 S‐tolerant fish differentially express genes and modify mitochondrial function to tolerate toxic levels of H 2 S relative to non‐tolerant fish. We have found that H 2 S‐tolerant fish differentially express SQR, VEGF, CSE, COX, and P450 (which are involved in H 2 S responses in other models) under control and H 2 S conditions relative to non‐tolerant fish. Furthermore, mitochondria isolated from H 2 S‐tolerant fish livers exhibit modifications in the coupling of electron transport and oxidative phosphorylation compared to non‐tolerant fish mitochondria. These data suggest that this is a valuable model to elucidate mechanisms involved in regulating H 2 S.