Effects of hydrogen sulfide exposure on lung mitochondrial respiratory chain enzymes in rats

Khan, A. A.; Schuler, Manuela; Prior, Michael G.; Yong, S.; Coppock, Robert W.; Florence, L.Z.; Lillie, L. E.

doi:10.1016/0041-008x(90)90321-k

Cited by 183 publications

(141 citation statements)

References 22 publications

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“…As has been suggested in literature, H 2 S exhibits its toxicity via inhibiting cellular metabolism by suppressing the respiratory chain in the mitochondria (32). Suppression of glucose-induced insulin release by L-cysteine and NaHS may result from their inhibition of glucose metabolism as shown by the fluorometrical measurements in the present study.…”

Section: Fig 6 Effects Of L-cysteine and Nahs On Casupporting

confidence: 55%

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

et al. 2006

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Hydrogen sulfide (H 2 S) was historically recognized as a toxic gas generated by natural resources. However, its enzymatic production from L-cysteine has recently been demonstrated in mammals. Cystathionine ␤-synthase and cystathionine ␥-lyase, both of which can produce H 2 S, were expressed in mouse pancreatic islet cells and the ␤-cell line, MIN6. L-Cysteine and the H 2 S donor NaHS inhibited glucose-induced insulin release from islets and MIN6 cells. These inhibitory effects were reproduced when insulin release was stimulated by ␣-ketoisocaproate, tolbutamide, or high K ؉

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Section: Fig 6 Effects Of L-cysteine and Nahs On Casupporting

confidence: 55%

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

et al. 2006

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“…However, it has recently been shown that complex I inhibition may underlie the cardioprotective effects of agents such as amobarbital [29,30], volatile anesthetics [60], and ranolazine [61]. Complex II inhibitors such as diazoxide [60] and 3-nitropropionic acid [62,63] are also cardioprotective, as are complex IV inhibitors such as hydrogen sulfide [64,65] and carbon monoxide [66]. In addition it is reported that glycolysis is inhibited in IPC [67], and it is known that a key regulator of glycolysis, GAPDH, is a target for S-nitrosation [68].…”

Section: Discussionmentioning

confidence: 99%

Cardioprotection and mitochondrial S-nitrosation: Effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia–reperfusion injury

Nadtochiy

Burwell

Brookes

2007

Journal of Molecular and Cellular Cardiology

132

118

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Mitochondrial dysfunction is a key pathologic event in cardiac ischemia-reperfusion (IR) injury, and protection of mitochondrial function is a potential mechanism underlying ischemic preconditioning (IPC). Acknowledging the role of nitric oxide (NO • ) in IPC, it was hypothesized that mitochondrial protein S-nitrosation may be a cardioprotective mechanism. The reagent S-nitroso-2-mercaptopropionyl-glycine (SNO-MPG) was therefore developed to enhance mitochondrial Snitrosation and elicit cardioprotection. Within cardiomyocytes, mitochondrial proteins were effectively S-nitrosated by SNO-MPG. Consistent with the recent discovery of mitochondrial complex I as an S-nitrosation target, SNO-MPG inhibited complex I activity and cardiomyocyte respiration. The latter effect was insensitive to the NO • scavenger c-PTIO, indicating no role for NO • -mediated complex IV inhibition. A cardioprotective role for reversible complex I inhibition has been proposed, and consistent with this SNO-MPG protected cardiomyocytes from simulated IR injury. Further supporting a cardioprotective role for endogenous mitochondrial S-nitrosothiols, patterns of protein S-nitrosation were similar in mitochondria isolated from Langendorff perfused hearts subjected to IPC, and mitochondria or cells treated with SNO-MPG. The functional recovery of perfused hearts from IR injury was also improved under conditions which stabilized endogenous S-nitrosothiols (i.e. dark), or by pre-ischemic administration of SNO-MPG. Mitochondria isolated from SNO-MPG-treated hearts at the end of ischemia exhibited improved Ca 2+ handling and lower ROS generation. Overall these data suggest that mitochondrial S-nitrosation and complex I inhibition constitute a protective signaling pathway that is amenable to pharmacologic augmentation.

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“…Dykens & Shick (1988) found that tolerance towards anoxic followed by normoxic incubation of clams was partly due to a low XDH tissue content. Khan et al (1990) postulated that the inhibition of cytochrome c-oxidase and of catalase by environmental sulfide in isolated mitochondria in vitro enhances the liberation of generated oxygen radicals and H202.…”

Section: Discussionmentioning

confidence: 99%

Biochemical adaptations of Nereis diversicolor (Polychaeta) to temporarily increased hydrogen peroxide levels in intertidal sandflats

Abele-Oeschger¹,

Oeschger²,

Theede³

1994

Mar. Ecol. Prog. Ser.

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Toxic hydrogen peroxide (H202] is photochemically generated in hyperoxic and normoxlc intertidal pools. Surprisingly high amounts of H202 penetrate the redoxcline, and are measurable in pore water in spite of the anoxic conditions prevailing there. Bioturbate macrofauna inhabiting these sediments encounters oxic conditions with peroxide in surface pools and anoxic conditions with peroxide in the sediment. We studied antioxidative properties in the polychaete Nereis diversicolor. Antioxidant enzyme activities of catalase and superoxide dismutase (SOD) showed annual variations correlated to the environmental peroxide concentrations. Epitokous specimens from April exhibited very high enzyme activities. Catalase was predominantly localised in the mitochondria and is inducible by peroxide incubation under experimental conditions. SOD activities were not inducible during oxic peroxide incubation. In contrast, SOD had higher activities when the worms were kept anoxically in the presence of hydrogen sulfide (100 pM) or hydrogen peroxide (5 PM). The radical stress the worms encountered during anoxic peroxide incubation was reflected by a highly increased lactate formation.Under oxic conditions 500 nM H202 decreased oxygen uptake of N. diversicolor by 38%. In epitokous N. diversicolor, this was accompanied by a conversion of heme to the green pigment biliverdin, a potent antioxidant. Billverdin was accumulated by the worms dunng oogenesis under natural conditions. Therefore its formation during spawning seems to be a response to increasing hydrogen peroxide concentrations in sediment pore water during spring. Biliverdin was not formed under anoxic conditions, because the conversion requires oxygen. Atokous worms lacked the ability to form biliverdin when exposed to peroxide.

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Effects of hydrogen sulfide exposure on lung mitochondrial respiratory chain enzymes in rats

Cited by 183 publications

References 22 publications

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

Cardioprotection and mitochondrial S-nitrosation: Effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia–reperfusion injury

Biochemical adaptations of Nereis diversicolor (Polychaeta) to temporarily increased hydrogen peroxide levels in intertidal sandflats

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