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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
While H2S is well known as a toxic gas through its inhibition of aerobic respiration, a recent paradigm shift in the research surrounding H2S has been inspired by the realization that it is an important signaling gas in the vasculature on a par with nitric oxide.997 H2S can serve as an inorganic source of energy to mammalian cells.998 3-Mercaptopyruvate sulfurtransferase (3MST) is expressed in the vascular endothelium, and it produces H2S derived from 3-mercaptopyruvate which stimulates additional mitochondrial H2S production, which then is oxidized to thiosulfate via at least three different pathways999–1001 and produces ATP. The inflammatory agent superoxide can act as substrate for the oxidation of H2S to sulfite and subsequently sulfate and the activated form PAPS1002 but will likely induce oxidative damage in the pancreas, particularly, as we will see in Section “Molybdenum Deficiency”, if molybdenum deficiency impairs sulfite-to-sulfate synthesis. The superoxide and H2S can constrict the microcirculation resulting in tissue hypoxia and metabolic acidosis.
Physiological and pathophysiological implications of hydrogen sulfide: a persuasion to change the fate of the dangerous molecule
Published in Journal of the Chinese Advanced Materials Society, 2018
Jan Mohammad Mir, Ram Charitra Maurya
Another important gaseous molecule, H2S was bearing the public image of a deadly ‘gas of rotten eggs,’ and known for hundreds of years as a toxicant.[20] It is a water soluble colorless gas and can cause a range of harmful effects even if present in a concentration as low as 0.05 ppm.[21] With the increasing concentration, it causes irritation in eyes and respiratory track and difficulty in breathing. Long-term exposure to low concentrations, even a few breaths of the gas at the concentration of 1000 ppm can prove lethal.[22–24] In and around 1990 the presence of H2S in tissues of rat brain and in normal human post-mortem brainstem resulted as a turning point for this gas. It has been now proved that the action of cysteine metabolic enzymes: cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) produces H2S endogenously in mammalian tissues at low micromolar levels.[25–27] H2S has been recognized to be involved in various physiological and pathological processes in human beings. It is now labeled as the third gasotransmitter after NO and CO.[28, 29] Biological membrane infiltrating ability of the molecule may be due to its small size and lipid solubility.[30, 31] Some key roles of this molecule have been shown in Figure 3. Recognition of the role of molecule in various body tissues, in inflammation and pain perception stems the fact that H2S is a member of gasotransmitters together with NO and CO.[32] But, much less is known about the physiological role of H2S than about either NO or CO. The importance of these gasotransmitters in the microbial world is advented from NO as an intermediate in denitrification[33] and is detoxified by pathogens,[34] CO is an unusual carbon and energy source,[35] and H2S is well known to all microbiologists as a product of anoxic sulfate respiration.[36] In addition to above, each gas is reported to have valuable therapeutic potential.[37]