Increased expression of stress proteins in the surf clam Donax variabilis following hydrogen sulfide exposure

Joyner-Matos, Joanna; Downs, Craig A.; Julian, David

doi:10.1016/j.cbpa.2006.06.033

Cited by 31 publications

(19 citation statements)

References 94 publications

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“…These findings are consistent with sulfide exposure causing increased free radical production and oxidative stress (Abele-Oeschger and Oeschger, 1995;Attene-Ramos et al, 2007;Chen and Morris, 1972;Eghbal et al, 2004;Joyner-Matos et al, 2006;Tapley, 1993;Tapley et al, 1999;Truong et al, 2006) and leads to the hypothesis that appropriate antioxidants could increase the viability of cells exposed to sulfide. To assess erythrocyte viability in the present study, we determined whether the cells became labeled with the fluorescent dyes calcein ) and exposed for 2 h to 0-3.2% H 2 S. N=5.…”

Section: J a Ortega J M Ortega And D Juliansupporting

confidence: 75%

Hypotaurine and sulfhydryl-containing antioxidants reduce H2S toxicity in erythrocytes from a marine invertebrate

Ortega

Julian

2008

Journal of Experimental Biology

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SUMMARYHypotaurine (HT) has been proposed to reduce sulfide toxicity in some deep-sea invertebrates by scavenging free radicals produced from sulfide oxidation or by scavenging sulfide via the reaction of HT with sulfide, forming thiotaurine (ThT). We tested whether HT or several antioxidants could reduce the total dissolved sulfide concentration in buffered seawater exposed to H 2 S, and whether HT, ThT or antioxidants could increase the viability of Glycera dibranchiata erythrocytes exposed to H 2 S in vitro. We found that 5 and 50 mmol l -1 HT reduced the dissolved sulfide in cell-free buffer exposed to H 2 S by up to 80% whereas the antioxidants glutathione ethyl ester (GEE) ), which contain sulfhydryl groups, increased cell viability during H 2 S exposure but to a lesser extent than HT whereas ASC, Tempol and Trolox, which do not contain sulfhydryl groups, decreased viability or had no effect. These data show that HT can protect cells from sulfide in vitro and suggest that sulfide scavenging, rather than free radical scavenging, is the most important mechanism of protection.,

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Section: J a Ortega J M Ortega And D Juliansupporting

confidence: 75%

Hypotaurine and sulfhydryl-containing antioxidants reduce H2S toxicity in erythrocytes from a marine invertebrate

Ortega

Julian

2008

Journal of Experimental Biology

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“…Reactive oxygen species formation was observed by others after sulfide treatment in cell cultures and tissue explants (38)(39)(40). To further test the hypothesis that oxidative species are involved in sulfide genotoxicity and to enhance the specificity of resulting DNA damage, we conducted experiments using [fapy]-DNA glycosylase (41).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Induces Direct Radical-Associated DNA Damage

Attene‐Ramos

Wagner

Gaskins

et al. 2007

Molecular Cancer Research

245

172

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Hydrogen sulfide (H 2 S) is produced by indigenous sulfate-reducing bacteria in the large intestine and represents an environmental insult to the colonic epithelium. Clinical studies have linked the presence of either sulfate-reducing bacteria or H 2 S in the colon with chronic disorders such as ulcerative colitis and colorectal cancer, although at this point, the evidence is circumstantial and underlying mechanisms remain undefined. We showed previously that sulfide at concentrations similar to those found in the human colon induced genomic DNA damage in mammalian cells. The present study addressed the nature of the DNA damage by determining if sulfide is directly genotoxic or if genotoxicity requires cellular metabolism. We also questioned if sulfide genotoxicity is mediated by free radicals and if DNA base oxidation is involved. Naked nuclei from untreated Chinese hamster ovary cells were treated with sulfide; DNA damage was induced by concentrations as low as 1 Mmol/L. This damage was effectively quenched by cotreatment with butylhydroxyanisole. Furthermore, sulfide treatment increased the number of oxidized bases recognized by formamidopyrimidine [fapy]-DNA glycosylase. These results confirm the genotoxicity of sulfide and strongly implicate that this genotoxicity is mediated by free radicals. These observations highlight the possible role of sulfide as an environmental insult that, given a predisposing genetic background, may lead to genomic instability or the cumulative mutations characteristic of colorectal cancer. (Mol Cancer Res 2007;5(5):455 -9)

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“…Previous studies demonstrated the induction of Hsp70 and sHSPs in a number of conditions leading to oxidative stress, including renal ischemia, intestinal hypoxiareoxygenation experiments (Gebhardt et al, 1999;Smoyer et al, 2000) and hypoxia exposure in Lymnaea stagnalis snails (Fei et al, 2007). In the surf clam Donax variabilis, hyperoxia induced the expression of Hsp70, whereas sulfide-induced oxidative damage induced the expression of sHSPs (Joyner-Matos et al, 2006). Hsp70 and Hsp27 have potential roles against cellular damage induced by oxidative stress Giffard et al, 2004;Huot et al, 1995;Mehlen et al, 1995), Hsp70 probably by acting as a molecular chaperone, whereas the protective effects of sHSPs were related to Z. Arad and others Hsp level (% change from aestivation) Fig.4.…”

Section: Hsps and Oxidative Stressmentioning

confidence: 97%

Natural annual cycle of heat shock protein expression in land snails: desertversusMediterranean species ofSphincterochila

Arad

Mizrahi

Goldenberg

et al. 2010

Journal of Experimental Biology

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SUMMARYLand snails are subject to daily and seasonal variations in temperature and in water availability, and have evolved annual cycles of activity and aestivation as part of their survival strategy. We tested in the field whether adaptation to different habitats affects the endogenous levels of heat shock proteins (HSPs) in two closely related Sphincterochila snail species, a desiccation-resistant desert species, Sphincterochila zonata, and a Mediterranean-type, desiccation-sensitive species, S. cariosa. We examined HSP levels in various tissues of snails during aestivation and after resumption of activity. Our study shows that, during aestivation, S. cariosa had higher standing stocks of Hsp70 in the foot and the hepatopancreas, and of small HSPs (sHSPs) in all the examined tissues, whereas S. zonata had higher stocks of Hsp70 in the kidney and of Hsp90 in the kidney and in the hepatopancreas. Arousal induced a general upregulation of HSPs, except for Hsp90, the expression of which in the foot was higher during aestivation. We suggest that the stress protein machinery is upregulated during arousal in anticipation of possible oxidative stress ensuing from the accelerating metabolic rate and the exit from the deep hypometabolic state. Our findings support the concept that, in land snails, aestivation and activity represent two distinct physiological states, and suggest that land snails use HSPs as important components of the aestivation mechanism, and as part of their survival strategy during and after arousal. Our study also indicates that adaptation to different habitats results in the development of distinct strategies of HSP expression with likely consequences for the ecology and distribution of land snails. Supplementary material available online at

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Increased expression of stress proteins in the surf clam Donax variabilis following hydrogen sulfide exposure

Cited by 31 publications

References 94 publications

Hypotaurine and sulfhydryl-containing antioxidants reduce H2S toxicity in erythrocytes from a marine invertebrate

Hypotaurine and sulfhydryl-containing antioxidants reduce H2S toxicity in erythrocytes from a marine invertebrate

Hydrogen Sulfide Induces Direct Radical-Associated DNA Damage

Natural annual cycle of heat shock protein expression in land snails: desertversusMediterranean species ofSphincterochila

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