Acido solfidrico nella letteratura internazionale

An inexpensive paper-based sensor was developed for detecting low ppm concentrations of hydrogen sulfide gas. A piece of filter paper containing aquohydroxocobinamide [OH(H2O)Cbi] was placed on the end of a bifurcated optical fiber, and the reflectance spectrum of the OH(H2O)Cbi was monitored during exposure to 10.0 ppm hydrogen sulfide gas (NIOSH recommended exposure limit). Reaction of sulfide (HS-) yielded an increase in reflectance from 400-450 nm, and decrease from 470-550 nm. Spectral changes were monitored as a function of time at 25, 50, and 85% relative humidity. Spectral shifts at high-er humidity suggested reduction of the Cbi(III) compound. The sensor was used to detect hydrogen sulfide breakthrough from respirator carbon beds and results correlated well with a standard electrochemical detector. The simple paper-based sensor could provide a real-time end-of-service-life alert for hydrogen sulfide gas (2) Cai J, Shi X, Wang H, Fan J, Feng Y, Lin X, et al. Cystathionine gamma lyase-hydrogen sulfide increases peroxisome proliferator-activated receptor gamma activity by sulfhydration at C139 site thereby promoting glucose uptake and lipid storage in adipocytes. Biochim Biophys Acta 2016 May;1861(5):419-29. Abstract: Adipocytes express the cystathionine gamma lyase (CSE)-hydrogen sulfide (H2S) system. CSE-H2S promotes adipogenesis but ameliorates adipocyte insulin resistance. We investigated the mechanism of how CSE-H2S induces these paradoxical effects. First, we confirmed that an H2S donor or CSE overexpression promoted adipocyte differentiation. Second, we found that H2S donor inhibited but CSE inhibition increased phosphodiesterase (PDE) activity. H2S replacing isobutylmethylxanthine in the differentiation program induced adipocyte differentiation in part. Inhibiting PDE activity by H2S induced peroxisome proliferator activated receptor gamma (PPARgamma) protein and mRNA expression. Of note, H2S directly sulfhydrated PPARgamma protein. Sulfhydrated PPARgamma increased its nuclear accumulation, DNA binding activity and adipogenesis gene expression, thereby increasing glucose uptake and lipid storage, which were blocked by the desulfhydration reagent DTT. H2S induced PPARgamma sulfhydration, which was blocked by mutation of the C139 site of PPARgamma. In mice fed a high-fat diet (HFD) for 4weeks, the CSE inhibitor decreased but H2S donor increased adipocyte numbers. In obese mice fed an HFD for 13weeks, H2S treatment increased PPARgamma sulfhydration in adipose tissues and attenuated insulin resistance but did not increase obesity. In conclusion, CSE-H2S increased PPARgamma activity by direct sulfhydration at the C139 site, thereby changing glucose into triglyceride storage in adipocytes. CSE-H2S-mediated PPARgamma activation might be a new therapeutic target for diabetes associated with obesity (3) Zhang S, Bian H, Li X, Wu H, Bi Q, Yan Y, et al. Hydrogen sulfide promotes cell proliferation of oral cancer through activation of the COX2/AKT/ERK1/2 axis. Oncol Rep 2016 May;35(5):2825-32. Abstract: Hydrogen sulfide, the third gaseous transmitter, is one of the main causes of halitosis in the oral cavity. It is generally considered as playing a deleterious role in many oral diseases including oral cancer. However, the regulatory mechanisms involved in the