Effects of Long-term Exposure to Hydrogen Sulfide on Human Red Blood Cells

Saeedi, Arastoo; Najibi, Asma; Mohammadi-Bardbori, Afshin

doi:10.15171/ijoem.2015.482

Cited by 49 publications

(31 citation statements)

References 33 publications

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“…Thus far, the formation of sulfheme is physiologically associated with sulfhemoglobinemia, a rare condition provoking oxygen desaturation and cyanosis and resulting from the long term exposure to H 2 S or sulfur-containing drug overdose5657. Also, the formation of sulfheme presumably occurs during the degradation of H 2 S in red blood cells58 and during the reactivity of red meat pigments with Cys-derived sulfhydryl radicals (S· − ) under the acidic conditions of the stomach59.…”

Section: Resultsmentioning

confidence: 99%

Sulfheme formation during homocysteine S-oxygenation by catalase in cancers and neurodegenerative diseases

et al. 2016

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Accumulating evidence suggests that abnormal levels of homocysteine are associated with vascular dysfunctions, cancer cell proliferation and various neurodegenerative diseases. With respect to the latter, a perturbation of transition metal homeostasis and an inhibition of catalase bioactivity have been reported. Herein, we report on some of the molecular bases for the cellular toxicity of homocysteine and demonstrate that it induces the formation of sulfcatalase, an irreversible inactive state of the enzyme, without the intervention of hydrogen sulfide. Initially, homocysteine reacts with native catalase and/or redox-active transition metal ions to generate thiyl radicals that mediate compound II formation, a temporarily inactive state of the enzyme. Then, the ferryl centre of compound II intervenes into the unprecedented S-oxygenation of homocysteine to engender the corresponding sulfenic acid species that further participates into the prosthetic heme modification through the formation of an unusual Fe(II) sulfonium. In addition, our ex cellulo studies performed on cancer cells, models of neurodegenerative diseases and ulcerative colitis suggest the likelihood of this scenario in a subset of cancer cells, as well as in a cellular model of Parkinson's disease. Our findings expand the repertoire of heme modifications promoted by biological compounds and point out another deleterious trait of disturbed homocysteine levels that could participate in the aetiology of these diseases.

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Section: Resultsmentioning

confidence: 99%

Sulfheme formation during homocysteine S-oxygenation by catalase in cancers and neurodegenerative diseases

et al. 2016

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“…In addition, Han et al have illustrated that oxidative stress could induce necroptosis during hyperoxic acute lung damage [46]. Besides, the activation of the NADPH oxidase systems or inhibition of mitochondrial respiration lead to the formation of a lot of H 2 O 2 in long-term H 2 S-exposed human red blood cells [47]. Here we have shown that, in contrast to control groups, the antioxidant ability was significantly impaired in H 2 S groups, and with the prolongation of the H 2 S exposure time, the antioxidation ability became weaker and weaker.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

Chi

Wang

2019

Oxidative Medicine and Cellular Longevity

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Hydrogen sulfide (H2S) is one of the main pollutants in the atmosphere, which is a serious threat to human health. The decomposition of sulfur-containing organics in chicken houses could produce a large amount of H2S, thereby damaging poultry health. In this study, one-day-old broilers were selected and exposed to 4 or 20 ppm of H2S gas (0-3 weeks: 4±0.5 ppm, 4-6 weeks: 20±0.5 ppm). The spleen samples were collected immediately after the chickens were euthanized at 2, 4, and 6 weeks. The histopathological and ultrastructural observations showed obvious necrosis characteristics of H2S-exposed spleens. H2S exposure suppressed GSH, CAT, T-AOC, and SOD activities; increased NO, H2O2, and MDA content and iNOS activity; and induced oxidative stress. ATPase activities and the expressions of energy metabolism-related genes were significantly decreased. Also, the expressions of related necroptosis (RIPK1, RIPK3, MLKL, TAK1, TAB2, and TAB3) were significantly increased, and the MAPK pathway was activated. Besides, H2S exposure activated the NF-κB classical pathway and induced TNF-α and IL-1β release. Taken together, we conclude that H2S exposure induces oxidative stress and energy metabolism dysfunction; evokes necroptosis; activates the MAPK pathway, eventually triggering the NF-κB pathway; and promotes inflammatory response in chicken spleens.

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“…The glutathione persulfide may be oxidized by ETHE1 and thiosulfate by TST to regenerate sulfite, which is oxidized by SO to sulfate [36,40,41]. Additionally, a part of H 2 S is exhaled or scavenged in the blood by methemoglobin to form sulfhemoglobin [42][43][44].…”

Section: H 2 S Excretionmentioning

confidence: 99%

Hydrogen Sulfide in Pharmacotherapy, Beyond the Hydrogen Sulfide-Donors

et al. 2020

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Hydrogen sulfide (H2S) is one of the important biological mediators involved in physiological and pathological processes in mammals. Recently developed H2S donors show promising effects against several pathological processes in preclinical and early clinical studies. For example, H2S donors have been found to be effective in the prevention of gastrointestinal ulcers during anti-inflammatory treatment. Notably, there are well-established medicines used for the treatment of a variety of diseases, whose chemical structure contains sulfur moieties and may release H2S. Hence, the therapeutic effect of these drugs may be partly the result of the release of H2S occurring during drug metabolism and/or the effect of these drugs on the production of endogenous hydrogen sulfide. In this work, we review data regarding sulfur drugs commonly used in clinical practice that can support the hypothesis about H2S-dependent pharmacotherapeutic effects of these drugs.

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Effects of Long-term Exposure to Hydrogen Sulfide on Human Red Blood Cells

Abstract: Long-term exposure to even low levels of H2S in workplaces may have potential harmful effects on human health.

Cited by 49 publications

References 33 publications

Sulfheme formation during homocysteine S-oxygenation by catalase in cancers and neurodegenerative diseases

Sulfheme formation during homocysteine S-oxygenation by catalase in cancers and neurodegenerative diseases

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

Hydrogen Sulfide in Pharmacotherapy, Beyond the Hydrogen Sulfide-Donors

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