Sulfeto de hidrogênio. Pode ser produzido por 3 tipos de enzimas

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Sulfeto de hidrogênio. Pode ser produzido por 3 tipos de enzimas nos
seres humanos no cérebro e no endotélio e possui forte efeito antioxidante
22/06/11
Uma das enzimas a 3-MST (3-mercaptopiruvato sulfurtransferase) está localizada principalmente nas mitocôndrias e possui
a importante função de reduzir as espécies reativas tóxicas de oxigênio geradas nesta organela, principal local de geração endógena
das ERTOS. Entretanto, o H2S intoxica a citocromo-oxidase de modo semelhante ao cianeto em concentrações sub-micromolares
(Antioxid Redox Signal. 2011 Apr 20). José de Felippe Junior
Mitochondria and Sulfide: A Very Old Story of Poisoning, Feeding, and Signaling?
Hydrogen sulfide: Its production and functions.
Kimura H.
Exp Physiol. 2011 Apr 28.
Source
National Institute of Neuroscience.
Abstract
Endogenous levels of sulfide in the brain has been measured in rats, humans and bovine in 1989 and 90, suggesting that H2S may have
a physiological function. We demonstrated in 1996 that cystathionine β synthase can produce H2S in the brain and that H2S facilitates
the induction of hippocampal long-term potentiation (LTP) by enhancing the activity of NMDA receptors. The following year we showed
that another H2S producing enzyme, cystathionine γ-lyase is expressed in the thoracic aorta, portal vein and ileum and that H2S
relaxes these tissues. We proposed that H2S may be a neuromodulator as well as a smooth muscle relaxant. In addition to a function
as a signaling molecule, we demonstrated another function as a cytoprotectant in 2004. H2S protects neurons from oxidative stress by
reinstating the reduced glutathione levels. We recently demonstrated that the third H2S producing enzyme, 3-mercaptopyruvate
sulfurtransferase (3MST) is expressed in neurons and vascular endothelium.
In addition to reinstating glutathione levels,
H2S produced by 3MST, which is mainly localized to mitochondria, reduces reactive oxygen species generated in this
organelle.
PMID:
21527544
24/10/2011 16:48
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