Hydrogen sulfide mechanism

A typical example of a nonpolymeric chain-propagating radical reaction is the anti-Markovnikov addition of hydrogen sulfide to a terminal olefin. The mechanism involves alternating abstraction and addition reactions in the propagating steps ... 

NKK s Bio-SR process is another iron-based redox process which instead of chelates, uses Thiobacillusferroidans )2iQ. - 2i to regenerate the solution (9). This process absorbs hydrogen sulfide from a gas stream into a ferric sulfate solution. The solution reacts with the hydrogen sulfide to produce elemental sulfur and ferrous sulfate. The sulfur is separated via mechanical means, such as filtering. The solution is regenerated to the active ferric form by the bacteria. 

In absence of oxygen some hydrogen does manage to evolve and polarize the cathode to some extent. However, if oxygen is present, this polarization does not occur as discussed earlier, and results in accelerated corrosion attack. Hydrogen sulfide ionizes in two main stages when dissolved in fluid. The reactions mechanisms are... 

Organisms also evolved powerful detoxifying mechanisms that remove toxic materials or convert them to non-toxic forms or nutrients. Examples of alterations to non-toxic forms are the conversions of hydrogen sulfide to sulfate and nitrite to nitrate. The prime example of development of the ability to use a toxic substance is the evolution of aerobic metabolism, which converted a serious and widespread toxin, oxygen, into a major resource. This development, as we have seen, greatly increased the productivity of the biosphere and generated the oxygen-rich atmosphere of today s Earth. 

Addition of hydrogen sulfide in solution was found to enhance the rate of this process albeit the efficiencies were generally low, partly due to concomitant precipitation of elemental sulfur during the photolytic experiments. The effects of reaction temperature, light intensity, and pH of the electrolyte were studied, and the photo-catalytic mechanism was discussed with reference to the theory of charge transfer at photoexcited metal sulfide semiconductors. 

These profiles clearly show that in the gas phase the alkylations of both ammonia and water by o-QM are assisted by an additional water molecule H-bonded to o-QM (water-catalyzed mechanism), since S4 and S5 TSs are favored over their uncatalyzed counterparts (SI and S2) by 5.6 and4.0 kcal/mol [at the B3LYP/6-311 + G(d,p) level], respectively. In contrast, the reaction with hydrogen sulfide in the gas phase shows a slight preference for a direct alkylation without water assistance (by 0.8 kcal/mol). 

These experts collectively have knowledge of hydrogen sulfide s physical and chemical properties, toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, and Liability Act, as amended. 

Inhibition of monoamine oxidase has been proposed as a possible mechanism underlying the hydrogen sulfide-mediated disruption of neurotransmission in brain stem nuclei controlling respiration (Warenycia et al. 1989a). Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide, has been shown to increase brain catecholamine and serotonin levels in rats. It has also been suggested that persulfide formation resulting from sulfide interaction with tissue cystine and cystinyl peptides may underlie some... 

The mechanism of hydrogen sulfide toxicity is in part similar to that of cyanide. Like cyanide, hydrogen sulfide can inhibit the enzyme cytochrome oxidase resulting in tissue hypoxia. Specific health effects are discussed in greater detail below. 

Alterations in blood heme metabolism have been proposed as a possible indicator of the biological effects of hydrogen sulfide (Jappinen and Tenhunen 1990), but this does not relate to the mechanism of toxicity in humans. The activities of the enzymes of heme synthesis, i.e., delta-aminolevulinic acid synthase (ALA-S) and heme synthase (Haem-S), were examined in 21 cases of acute hydrogen sulfide toxicity in Finnish pulp mill and oil refinery workers. Subjects were exposed to hydrogen sulfide for periods ranging from approximately 1 minute to up to 3.5 hours. Hydrogen sulfide concentrations were considered to be in the range of 20-200 ppm. Several subjects lost consciousness for up to 3 minutes. 

Effect. Potential biomarkers of the subclinical effects of hydrogen sulfide are decreases in the activities of the heme synthesis enzymes, ALA-S and Haem-S (Jappinen and Tenhunen 1990). These effects have nothing to do with the mechanism of toxicity, however. Neurological indices are also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987 Kilbum 1993 Stine et al. 1976 Tvedt et al. 1991b). 

Freireich AW. 1946. Hydrogen sulfide poisoning Report of two cases, one with fatal outcome, from associated mechanical asphyxia. Am J Pathol 22 147-155. 

Nicholson RA, Roth SH, Jian Zheng AZ. 1998. Inhibition of respiratory and bioenergetic mechanisms by hydrogen sulfide in mammalian brain. J Toxicol Environ Health. 54 491-507. 

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