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Hydrogen Sulfide Induces Oxidative Damage to RNA and DNA in a Sulfide‐Tolerant Marine Invertebrate

Hydrogen sulfide acts as an environmental toxin across a range of concentrations and as a cellular signaling molecule at very low concentrations. Despite its toxicity, many animals, including the mudflat polychaeteGlycera dibranchiata, are periodically or continuously exposed to sulfide in their env...

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Published in:Physiological and biochemical zoology 2010-03, Vol.83 (2), p.356-365
Main Authors: Joyner‐Matos, Joanna, Predmore, Benjamin L., Stein, Jenny R., Leeuwenburgh, Christiaan, Julian, David
Format: Article
Language:English
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Summary:Hydrogen sulfide acts as an environmental toxin across a range of concentrations and as a cellular signaling molecule at very low concentrations. Despite its toxicity, many animals, including the mudflat polychaeteGlycera dibranchiata, are periodically or continuously exposed to sulfide in their environment. We tested the hypothesis that a broad range of ecologically relevant sulfide concentrations induces oxidative stress and oxidative damage to RNA and DNA inG. dibranchiata. Coelomocytes exposed in vitro to sulfide (0–3 mmol L−1for 1 h) showed dose‐dependent increases in oxidative stress (as 2′,7′‐dichlorofluorescein fluorescence) and superoxide production (as dihydroethidine fluorescence). Coelomocytes exposed in vitro to sulfide (up to 0.73 mmol L−1for 2 h) also acquired increased oxidative damage to RNA (detected as 8‐oxo‐7,8‐dihydroguanosine) and DNA (detected as 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine). Worms exposed in vivo to sulfide (0–10 mmol L−1for 24 h) acquired elevated oxidative damage to RNA and DNA in both coelomocytes and body wall tissue. While the consequences of RNA and DNA oxidative damage are poorly understood, oxidatively damaged deoxyguanosine bases preferentially bind thymine, causing G‐T transversions and potentially causing heritable point mutations. This suggests that sulfide can be an environmental mutagen in sulfide‐tolerant invertebrates.
ISSN:1522-2152
1537-5293
DOI:10.1086/597529