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Enhanced Spare Respiratory Capacity in Extremophile Fish Following Exposure to Hydrogen Sulfide
Author(s) -
Henpita Chathurika R,
Tobler Michael,
Shaw Jennifer H
Publication year - 2017
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.31.1_supplement.624.7
Subject(s) - population , biology , hydrogen sulfide , sulfide , chemistry , cytochrome c oxidase , mitochondrion , biochemistry , environmental chemistry , medicine , sulfur , environmental health , organic chemistry
Hydrogen sulfide (H 2 S) is well known as an environmental toxic gas produced by the decomposition of organic matter and geothermal sources. H 2 S is also produced endogenously in organisms as a result of cysteine catabolism. Exposure to H 2 S drives hormetic effects including the toxic inhibition of cytochrome c oxidase of the mitochondrial respiratory chain at high concentrations, and maintenance of normal vascular and neural functions at low concentrations. Physiological levels of H 2 S are necessary for blood pressure regulation, angiogenesis, and mitigating oxidative and inflammatory stress. Abnormal elevation of cellular H 2 S is correlated with vascular, metabolic and neurological dysfunction in most terrestrial and aquatic organisms, however there are some organisms such as the lugworm ( Arenicola marina ), tubeworms ( Riftia pachyptila ) and Atlantic molly ( Poecilia mexicana ) that thrive in extreme environments with high H 2 S concentrations. The mechanisms whereby organisms can tolerate extreme H 2 S are not fully understood. Since mitochondria are both the site of H 2 S toxicity as well as enzymatic detoxification, we sought to compare mitochondrial function in P. mexicana fish derived from two populations: sulfide‐tolerant and non‐tolerant, depending on the presence or absence of H 2 S in their habitat. We hypothesized that sulfide‐tolerant fish would reduce their oxygen consumption relative to the non‐tolerant population following H 2 S exposure. We further hypothesized that the wild captured sulfide‐tolerant population would maintain a greater degree of H 2 S tolerance compared to the lab‐reared sulfide‐tolerant population, which has not been exposed to H 2 S in several generations. Mitochondrial oxygen consumption rate (OCR) was measured in tolerant and non‐tolerant populations following seven doses of NaSH (H 2 S donor) using the Seahorse Biosciences XF e 96 coupling assay. Our key findings are that mitochondria from sulfide‐tolerant fish exhibited, i) a reduction in OCR under basal conditions and following exposure to low concentrations of H 2 S, ii) an increase in spare respiratory capacity following exposure to high concentrations of H 2 S and, iii) a greater degree of tolerance in the wild captured population, relative to lab‐reared.