Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication: increases in brain catecholamine and 5-hydroxytryptamine levels

Warenycia, Marcus W.; Smith, K. A.; Blashko, C. S.; Kombian, Samuel B.; Reiffenstein, R. J.

doi:10.1007/bf00316435

Cited by 64 publications

(32 citation statements)

References 21 publications

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“…H 2 S increases the levels of neurotransmitters c-amino butyric acid (GABA), glutamate, serotonin, dopamine, epinephrine, and norepinephrine (33). The levels of serotonin and catecholamine are increased by inhibition of monoamine oxidase (MAO) (74). H 2 S also enhances the effect of acetylcholine by suppressing the activity of its degradation enzyme, acetylcholinesterase.…”

Section: Synaptic Modulationmentioning

confidence: 99%

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Kimura

Shibuya²,

Kimura³

2012

Antioxidants & Redox Signaling

255

190

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Significance: Accumulating evidence shows that hydrogen sulfide may function as a signaling molecule in processes such as neuromodulation in the brain and smooth muscle relaxation in the vascular system. It also has a cytoprotective effect, since it can protect neurons and cardiac muscle from oxidative stress and ischemiareperfusion injury, respectively. Hydrogen sulfide can also modulate inflammation, insulin release, and angiogenesis. Recent Advances: The regulation of the activity of 3-mercaptopyruvate sulfur transferase (3MST) along with cysteine aminotransferase (CAT), one of the H 2 S producing pathways, has been demonstrated. The production of H 2 S by the pathway, which is regulated by Ca 2+ and facilitated by thioredoxin and dihydrolipoic acid, is also involved in H 2 S signaling as well as cytoprotection. Sulfur hydration of proteins by H 2 S has been proposed to modulate protein functions. H 2 S-sensitive fluorescent probes, which enable us to measure the localization of H 2 S in real time, have been developed. Critical Issues: The basal concentrations of H 2 S have recently been measured and found to be much lower than those initially reported. However, the concentration of H 2 S reached in stimulated cells, as well as the regulation of H 2 S producing enzymes is not well understood. It has been proposed that some of the effects of H 2 S on the regulation of enzymes and receptors might be explained through the properties of sulfane sulfur (S 0 ), another form of active sulfur. Future Directions: The determination of H 2 S concentrations in activated cells using new methods including H 2 S-sensitive fluorescent probes, as well as the investigation of the effects of H 2 S using specific inhibitors, may provide better understanding of the physiological function of this molecule. Clarifying mechanisms of H 2 S activity may also facilitate the development of new therapeutic compounds. Antioxid. Redox Signal. 17, 45-57.

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Section: Synaptic Modulationmentioning

confidence: 99%

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Kimura

Shibuya²,

Kimura³

2012

Antioxidants & Redox Signaling

255

190

View full text Add to dashboard Cite

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“…This theory would support the concept that H 2 S is a broad-spectrum toxicant (Roth, 1993). In support of the diverse biological actions of sulfide, other reports have documented sulfide-mediated inhibition of monoamine oxidase (Warenycia et al, 1989), cholinesterase, and Na + /K + -ATPase (Reiffenstein et al, 1992) in rat brain. The lack of an effective antidote to H 2 S poisoning also appears consistent with multiple mechanisms of action (Reiffenstein et al, 1992).…”

mentioning

confidence: 74%

Inhibition of Respiratory and Bioenergetic Mechanisms by Hydrogen Sulfide in Mammalian Brain

Nicholson

Roth²,

Zhang³

et al. 1998

Journal of Toxicology and Environmental Health, Part A

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The biochemical effects of hydrogen sulfide were investigated by treating enzyme homogenates and synaptosomes prepared from mammalian brain with sodium sulfide. Brain cytochrome c oxidase activity was highly sensitive to inhibition by sodium sulfide, as demonstrated by an IC50 of 0.13 microM. Sodium sulfide was also found to inhibit carbonic anhydrase activity in cerebellum, frontal cortex, and hippocampus. Synaptosomal oxygen consumption was significantly reduced as the concentration of sodium sulfide was increased from 20 to 100 microM; this was accompanied by a concentration-dependent depolarization of the synaptosomal mitochondrial membrane in situ and a reduction in synaptosomal ATP concentration. In other experiments using synaptosomes, sodium sulfide caused a significant calcium-independent increase in the extracellular accumulation of L-glutamate, inhibited Na+-dependent uptake of [3H]glutamate, but was unable to influence intrasynaptosomal free ionic Ca2+. Parallel studies conducted in vivo showed that rats exposed over a 5-d period to hydrogen sulfide (100 ppm for 3 h/d) had significantly higher concentrations of L-glutamate in the hippocampus compared to control animals. In summary, our results indicate that sulfide causes extensive disruption to respiratory and related mitochondrial functions in mammalian brain in vitro. The reduced capacity of nerve endings to take up L-glutamate may contribute to the raised L-glutamate levels observed in vivo.

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“…Since NaHS was considered a toxic substance, we injected NaHS (14 μmol/kg body weight/day) alone to control rats (n = 7) as the treatment control. Warenycia et al [30] reported an LD50 value of 15 mg/ kg body weight (approximately 192 μmol/kg body weight) for NaHS in rats, which is higher than the dosage we used. Another control group (n = 7) was supplied with sulphurous mineral water to exclude any toxic effect of H 2 S-rich water consumption.…”

Section: Experimental Designmentioning

confidence: 87%

“…Many studies have indicated that exogenous administration of the H 2 S donor NaHS to rats with myocardial injury reduces the mortality rate and the accumulation of plasmatic lipid peroxidation markers such as malondialdehyde (MDA) and conjugated dienes. At the same time, H 2 S may inhibit the formation of protein carbonyls induced in vitro by hypochlorous acid [30,71].…”

Section: Figmentioning

confidence: 99%

The Antiapoptotic Effects of Sulphurous Mineral Water and Sodium Hydrosulphide on Diabetic Rat Testes

Sadik

Elseweidy

Shaker

2011

Cell Physiol Biochem

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Background/Aims: It is well known that diabetes mellitus is associated with the impairment of testicular function. In the present study, we aimed to study the effects of sulphurous mineral water or sodium hydrosulphide (NaHS) on apoptotic testicular damage in rats with streptozotocin (STZ)-induced diabetes. Methods: Sulphurous mineral water (as drinking water) or NaHS (14 µmol/kg body weight/day, I.P.) was administered for 7 wks to rats with STZ-induced diabetes. Results: Hyperglycaemia, an overproduction of glycated haemoglobin (HbA1C) and a decline in serum insulin, C-peptide and insulin-like growth factor-I (IGF-I) were observed in diabetic rats. A decline in the serum testosterone level and an impairment of spermatogenesis, as indicated by a histopathological examination of diabetic rats, demonstrated significant testicular damage. Sulphurous mineral water and NaHS treatment may have improved the level of testicular GSH by blocking the overexpression of some apoptosis-related regulatory proteins such as Bax/Bcl-2, cytochrome c, caspase-9 and -3, and p53. This anti-apoptotic potential was associated with an increase in serum testosterone level and the amelioration of hyperglycaemia-related biochemical parameters. The histopathological examination was in harmony with the biochemical and molecular findings. Conclusion: Our study provides the first indication that sulphurous mineral water and NaHS may have a novel anti-apoptotic potential that could be a useful treatment in preventing diabetes-induced testicular dysfunction.

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Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication: increases in brain catecholamine and 5-hydroxytryptamine levels

Cited by 64 publications

References 21 publications

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Inhibition of Respiratory and Bioenergetic Mechanisms by Hydrogen Sulfide in Mammalian Brain

The Antiapoptotic Effects of Sulphurous Mineral Water and Sodium Hydrosulphide on Diabetic Rat Testes

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