Hydrogen Sulfide Intoxication with Dilated Cardiomyopathy

Lee, Eui-Cheol; Kwan, Jun; Leem, Jong-Han; Park, Shin-Goo; Kim, Hwan‐Cheol; Lee, Dong‐Hoon; Kim, Jeong-Hoon; Kim, Dong‐Hyun

doi:10.1539/joh.n9004

Cited by 11 publications

(12 citation statements)

References 14 publications

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“…People exposed to hydrogen sulfide at concentrations above 100 to 150 ppm may lose the ability to smell hydrogen sulfide after 2 to 15 min of continuous exposure due to olfactory fatigue. 310,311 Hydrogen sulfide is produced from sewage sludge, liquid manure, sulfur hot springs, and natural gas. It is also is a byproduct of various industrial processes such as petroleum refining, wood pulp processing, rayon manufacturing, manure processing, sugar beet processing, fish processing, and hot asphalt paving.…”

Section: Hydrogen Sulfidementioning

confidence: 99%

“…It is also is a byproduct of various industrial processes such as petroleum refining, wood pulp processing, rayon manufacturing, manure processing, sugar beet processing, fish processing, and hot asphalt paving. 310 The mechanism of its toxicity is via interruption of mitochondrial cellular respiration through inactivation of cytochrome oxidase. 310,311 Patients with hydrogen sulfide poisoning may present with mucosal damage, hemoptysis, tachycardia, cyanosis, lactic acidosis, and loss of consciousness.…”

Section: Hydrogen Sulfidementioning

confidence: 99%

“…310 The mechanism of its toxicity is via interruption of mitochondrial cellular respiration through inactivation of cytochrome oxidase. 310,311 Patients with hydrogen sulfide poisoning may present with mucosal damage, hemoptysis, tachycardia, cyanosis, lactic acidosis, and loss of consciousness. Myocardial infarction, myocarditis, and dilated cardiomyopathy have all been described following hydrogen sulfide exposure.…”

Section: Hydrogen Sulfidementioning

confidence: 99%

“…Myocardial infarction, myocarditis, and dilated cardiomyopathy have all been described following hydrogen sulfide exposure. 310 Detection of hydrogen sulfide in patients suspected of exposure can be accomplished with measurement of thiosulfate levels via chromatography of the blood or tissue. 311,312 Victims of hydrogen sulfide poisoning should be removed from the site of exposure, and oxygen should be administered.…”

Section: Hydrogen Sulfidementioning

confidence: 99%

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Environmental Toxins and the Heart

2015

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Section: Hydrogen Sulfidementioning

confidence: 99%

Section: Hydrogen Sulfidementioning

confidence: 99%

Section: Hydrogen Sulfidementioning

confidence: 99%

Section: Hydrogen Sulfidementioning

confidence: 99%

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Environmental Toxins and the Heart

2015

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“…Oxidative stress has been implicated in the development of many diseases including aging process and longevity [57], including the pathogenesis of Alzheimer's disease (AD) [58], Parkinson's disease (PD) [59] and other neurodegenerative diseases [60]. Physiological concentrations of H 2 S gas have positive impact on protecting the neuronal cells and the supply of exogenous H 2 S have shown attenuation effect on some brain diseases [61,62]. As such, the antioxidant role of H 2 S is attracting substantial research attention in addition to other gaseous messenger molecules such as nitrate monoxide (NO) and carbon monoxide (CO) [51].…”

Section: Proposed Mechanisms Of Sulfur-induced Pemmentioning

confidence: 99%

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Amat

Olkowski²,

Atila³

et al. 2013

Vet Med Anim Sci

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Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is an important neurologic disease that affects ruminants. Thiamine deficiency and sulfur (S) toxicity have been well recognized as major etiological factors. The mechanism of thiamine deficiency associated PEM has been well elucidated. However, the role of S in PEM pathogenesis remains unclear, although the relationship between S toxicity and PEM has been established for 3 decades. The development of S-induced malacic lesions is believed to be independent of thiamine deficiency, since blood thiamine levels in affected individuals remain in the range of normal animals. However, cattle affected by S-induced PEM frequently respond to thiamine treatment in early disease stages. Thiamine supplementation is reported to reduce the incidence and severity of S-induced PEM. This suggests a possible metabolic relationship between excess S intake and thiamine in the development of malacic lesions. Such an association is further supported by recent studies reporting that high dietary S may increase the metabolic demand for thiamine pyrophosphate (TPP), a critical cofactor in several metabolic pathways. Systemic failure to synthesize metabolically requisite levels of TPP in the brain may be an important precursor in the pathogenesis of S-induced PEM. There is increasing evidence of the importance of thiamine in the pathogenesis of S-induced PEM. Thus, understanding the potential role of S-thiamine interaction in the development of malacic lesions is important step to determine the mechanism of S-induced PEM. The objective of this article is to provide an overview of thiamine deficiency and S toxicity associated PEM, and to discuss the potential role of S-thiamine interaction in the pathogenesis of S-induced PEM in ruminants.

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