Hydrogen sulfide intoxication

Guidotti, Tee L.

doi:10.1016/b978-0-444-62627-1.00008-1

Cited by 64 publications

(74 citation statements)

References 115 publications

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“…The goal of this study was to develop a rodent model of H 2 S‐induced neurotoxicity, with a relevant route to human exposure, for characterizing mechanisms of H 2 S‐induced neurotoxicity and for use in translational studies aimed at evaluating the efficacy of countermeasures against H 2 S neurotoxicity . This study has led to the development of a novel inhalation mouse model of H 2 S‐induced neurotoxicity and neurodegeneration that recapitulates many of the features of the human condition, including clinical signs, behavioral responses, and neurodegeneration . There have been some recent attempts at developing such models, but the routes of H 2 S exposure employed were not relevant to chemical terrorism or farm/industrial H 2 S exposure.…”

Section: Discussionmentioning

confidence: 99%

Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide–induced neurotoxicity and neurological sequelae

Anantharam

Whitley²,

Mahama

et al. 2017

Annals of the New York Academy of Sciences

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Hydrogen sulfide (H S) is a highly neurotoxic gas. It is the second most common cause of gas-induced deaths. Beyond mortality, surviving victims of acute exposure may suffer long-term neurological sequelae. There is a need to develop countermeasures against H S poisoning. However, no translational animal model of H S-induced neurological sequelae exists. Here, we describe a novel mouse model of H S-induced neurotoxicity for translational research. In paradigm I, C57/BL6 mice were exposed to 765 ppm H S for 40 min on day 1, followed by 15-min daily exposures for periods ranging from 1 to 6 days. In paradigm II, mice were exposed once to 1000 ppm H S for 60 minutes. Mice were assessed for behavioral, neurochemical, biochemical, and histopathological changes. H S intoxication caused seizures, dyspnea, respiratory depression, knockdowns, and death. H S-exposed mice showed significant impairment in locomotor and coordinated motor movement activity compared with controls. Histopathology revealed neurodegenerative lesions in the collicular, thalamic, and cortical brain regions. H S significantly increased dopamine and serotonin concentration in several brain regions and caused time-dependent decreases in GABA and glutamate concentrations. Furthermore, H S significantly suppressed cytochrome c oxidase activity and caused significant loss in body weight. Overall, male mice were more sensitive than females. This novel translational mouse model of H S-induced neurotoxicity is reliable, reproducible, and recapitulates acute H S poisoning in humans.

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Section: Discussionmentioning

confidence: 99%

Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide–induced neurotoxicity and neurological sequelae

Anantharam

Whitley²,

Mahama

et al. 2017

Annals of the New York Academy of Sciences

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“…For the purposes of this paper, the term H 2 S will be used to refer to both species of H 2 S in vivo . Among toxic gases, H 2 S is the second most common cause of human death after carbon monoxide poisoning . High acute exposure to H 2 S leads to severe toxic effects, including death, with most deaths occurring at the scene of exposure .…”

Section: Introductionmentioning

confidence: 99%

Cobinamide is effective for treatment of hydrogen sulfide–induced neurological sequelae in a mouse model

Anantharam

Whitley²,

Mahama

et al. 2017

Annals of the New York Academy of Sciences

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Hydrogen sulfide (H2S) is a highly neurotoxic gas. Acute exposure can lead to neurological sequelae among survivors. A drug for treating neurological sequelae in survivors of acute H2S intoxication is needed. Using a novel mouse model we evaluated the efficacy of cobinamide (Cob) for this purpose. There were two objectives: (1) to determine the dose–response efficacy of Cob and (2) to determine the effective therapeutic time window of Cob. To explore objective 1, mice were injected intramuscularly with Cob at 0, 50 or 100 mg/kg at 2 min after H2S exposure. For objective 2, mice were injected intramuscularly with 100 mg/kg Cob at 2, 15, and 30 min after H2S exposure. For both objectives, mice were exposed to 765 ppm of H2S gas. Cob significantly reduced H2S-induced lethality in a dose-dependent manner (P < 0.05). Cob-treated mice exhibited significantly fewer seizures and knockdowns compared with the H2S-exposed group. Cob also reversed H2S-induced weight loss, behavioral deficits, neurochemical changes, cytochrome c oxidase enzyme inhibition, and neurodegeneration in a dose- and time-dependent manner (P < 0.01). Overall, these findings show that Cob increases survival and is neuroprotective in a mouse model of H2S-induced neurological sequelae.

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“…This gas is emitted from a number of natural and industrial sources, including geothermal areas, oil and gas fields and refineries, sewage treatment plants, and confined animal feeding operations (CAFOs or “factory farms”) (Lewis and Copley, 2015). It is also endogenously produced in humans and animals by gut bacteria and by the cells of some organs, where it has important physiological functions(Guidotti, 2015). H 2 S has a “rotten egg” smell, with a detection threshold of 10 ppb or lower.…”

Section: Introductionmentioning

confidence: 99%

Ambient geothermal hydrogen sulfide exposure and peripheral neuropathy

Pope

Crane

et al. 2017

NeuroToxicology

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The mechanism of toxicity of hydrogen sulfide (H2S) gas is thought mainly to operate through effects on the nervous system. The gas has high acute toxicity, but whether chronic exposure causes effects, including peripheral neuropathy, is yet unclear. The city of Rotorua, New Zealand, sits on an active geothermal field and the population has some of the highest measured ambient H2S exposures. A previous study in Rotorua provided evidence that H2S is associated with peripheral neuropathy. Using clinical methods, the present study sought to investigate and possibly confirm this association in the Rotorua population. The study population comprised 1,635 adult residents of Rotorua, aged 18–65. Collected data relevant to the peripheral neuropathy investigation included symptoms, ankle stretch reflex, vibration sensitivity, as measured by the timed-tuning fork test and a Bio-Thesiometer (Bio-Medical Instrument Co., Ohio), and light touch sensitivity measured by monofilaments. An exposure metric, estimating time-weighted H2S exposure across the last 30 years was used. Principal components analysis was used to combine data across the various indicators of possible peripheral neuropathy. The main data analysis used linear regression to examine associations between the peripheral nerve function indicators and H2S exposure. None of the peripheral nerve function indicators were associated with H2S exposure, providing no evidence that H2S exposure at levels found in Rotorua is a cause of peripheral neuropathy. The earlier association between H2S exposure and peripheral neuropathy diagnoses may be attributable to the ecological study design used. The possibility that H2S exposure misclassification could account for the lack of association found cannot be entirely excluded.

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Hydrogen sulfide intoxication

Cited by 64 publications

References 115 publications

Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide–induced neurotoxicity and neurological sequelae

Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide–induced neurotoxicity and neurological sequelae

Cobinamide is effective for treatment of hydrogen sulfide–induced neurological sequelae in a mouse model

Ambient geothermal hydrogen sulfide exposure and peripheral neuropathy

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