Hydrogen sulfide research from independent scientists...

The  papers provided below were selected from the work of world-renowned researchers* investigating the biological properties and therapeutic potential of hydrogen sulfide. Published in journals such as Nature Scientific Reports, the British Journal of Pharmacology and the Proceedings of the National Academy of Sciences (PNAS), they provide insight into the physiological significance of hydrogen sulfide across the animal and plant kingdoms.


* Note that these authors are not affiliated with Antibe Therapeutics.

November 2019

High-fat diet-mediated dysbiosis exacerbates NSAID-induced small intestinal damage through the induction of interleukin-17A

NSAIDs cause damage in the small intestine in a bacteria-dependent manner. As high-fat diet (HFD) is a potent inducer of gut dysbiosis, we investigated the effects of HFD on bacterial flora in the small intestine and NSAID-induced enteropathy. HFD-fed mice exhibited increased susceptibility to NSAID-induced damage in the small intestine; this phenotype was observed in normal diet-fed mice that received small intestinal microbiota from HFD-fed mice. Administration of neutralizing antibodies to HFD-fed mice reduced intestinal permeability and prevented exacerbation of NSAID-induced damage. Thus, HFD-induced microbial dysbiosis in small intestine caused microinflammation and increase in intestinal permeability, resulting in the aggravation of NSAID-induced small intestinal damage.


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January 2016

The Role of Hydrogen Sulfide in Evolution and the Evolution of Hydrogen Sulfide in Metabolism and Signaling

The chemical versatility of sulfur and its abundance in the prebiotic Earth as reduced sulfide (H2S) implicate this molecule in the origin of life 3.8 billion years ago and also as a major source of energy in the first seven-eighths of evolution. This article provides an in-depth review of the origins of hydrogen sulfide’s physiological functions, also explaining its unique role as a signalling molecule and metabolic regulator, including its anti-inflammatory properties.

OLSON KR, STRAUB KD, PHYSIOLOGY

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April 2012

Hydrogen sulfide and nitric oxide are mutually dependent in the regulation of angiogenesis and endothelium-dependent vasorelaxation

Hydrogen sulfide (H2S) is a unique gasotransmitter, with regulatory roles in the cardiovascular, nervous, and immune systems. Some of the vascular actions of H2S (stimulation of angiogenesis, relaxation of vascular smooth muscle) resemble those of nitric oxide (NO). Although it was generally assumed that H2S and NO exert their effects via separate pathways, the results of the current study show that H2S and NO are mutually required to elicit angiogenesis and vasodilatation.

COLETTA ET AL., PNAS

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February 2011

Hydrogen Sulfide and Cell Signaling

Hydrogen sulfide (H2S) is a gaseous mediator synthesized from cysteine by cystathionine ? lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H2S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel caliber, cardiac response to ischemia/reperfusion injury, and inflammation.

LI ET AL., ANNUAL REVIEW OF PHARMACOLOGY & TOXICOLOGY

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December 2010

Hydrogen sulphide and angiogenesis: mechanisms and applications

In vascular tissues, hydrogen sulphide (H2S) is mainly produced from L-cysteine by the cystathionine gamma-lyase (CSE) enzyme. Recent studies show that administration of H2S to endothelial cells in culture stimulates cell proliferation, migration and tube formation. Angiogenesis, the formation of new blood vessels, is crucial in the early stage of wound healing. Pharmacological modulation of H2S-mediated angiogenic pathways may open the door for novel therapeutic approaches.

SZABO ET AL., BRITISH JOURNAL OF PHARMACOLOGY

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August 2007

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.

ELROD ET AL., PNAS

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September 2005

Activation of KATP channels by H2S in rat insulin-secreting cells and the underlying mechanisms

H2S is an important gasotransmitter, generated in mammalian cells from L-cysteine metabolism. As it stimulates KATP channels in vascular smooth muscle cells, H2S may also function as an endogenous opener of KATP channels in INS-1E cells, an insulin-secreting cell line. Interaction among H2S, glucose and the KATP channel may constitute an important and novel mechanism for the fine control of insulin secretion from pancreatic ?-cells.

YANG ET AL., JOURNAL OF PHYSIOLOGY

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November 2002

Two’s company, three’s a crowd: can H2S be the third endogenous gaseous transmitter?

The endogenous metabolism and physiological functions of hydrogen sulfide (H2S) position this gas well in the novel family of endogenous gaseous transmitters, termed “gasotransmitters.” This positioning of H2S will open an exciting field—H2S physiology—encompassing realization of the interaction of H2S and other gasotransmitters, sulfurating modification of proteins, and the functional role of H2S in multiple systems. It may shed light on the pathogenesis of many diseases related to the abnormal metabolism of H2S.

WANG, FASEB

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July 2002

Hydrogen Sulfide in Biochemistry and Medicine

An abundance of experimental evidence suggests that hydrogen sulfide (H2S) plays a prominent role in physiology and pathophysiology. Many targets exist for H2S therapy. The molecular targets of H2S include proteins, enzymes, transcription factors, and membrane ion channels. Novel H2S precursors are being synthesized and discovered that are capable of releasing H2S in a slow and sustained manner. This presents a novel and advantageous approach to H2S therapy for treatment of chronic conditions associated with a decline in endogenous H2S, such as diabetes and cardiovascular disease.

PREDMORE ET AL., ANTIOXIDANTS & REDOX SIGNALING

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