| Reference | [1]. Environ Sci Technol. 2007 Mar 1;41(5):1735-9. doi: 10.1021/es062455f.<br />
Novel mercury control technology for solid waste incineration: sodium tetrasulfide (STS) as mercury capturing agent.<br />
Liu Y(1), Xie S, Li Y, Liu Y.<br />
Author information: (1)College of Environmental Sciences, Peking University, Beijing 100871, China. [email protected]<br />
Traditional pollution control technologies are able to capture oxidized forms of mercury to some extent; however, they show low efficiency for the control of elemental mercury emissions. This study developed a novel mercury removal technology: injection of sodium tetrasulfide (Na2S4) dissolved in the sodium hydroxide (NaOH) solution in the spray-dryer system. The effects of flue gas temperature and Na2S4 level in flue gas on the mercury removal efficiency were investigated. Na2S4 was decomposed into Na2S (S2-) and elemental S (S0), which reacted with HgCl2 and elemental Hg (Hg0), and HgS was then formed. Under the optimized operation parameters, this technology can simultaneously remove over 88% of HgCl2 and more than 90% of Hg0 from a flue gas stream containing about 400 microg m(-3) Hg0 and 1200 microg m(-3) HgCl2. The increased flue gas temperature (>170 degrees C) and the decreased Na2S4-to-Hg mass ratio (S-Hg-R) (<2.0) had negative effects on the reactions of gaseous mercury (HgCl2 + Hg0) with ionic sulfur (S2-) and S0. All the experiments were conducted in a full scale hospital-waste incinerator with a capability of 20 tons per day (TPD).<br />
DOI: 10.1021/es062455f PMID: 17396668<br />
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[2]. Virology. 1964 Feb;22:253-61. doi: 10.1016/0042-6822(64)90010-8.<br />
STABILIZATION OF POLIOVIRUS BY SODIUM TETRASULFIDE.<br />
PONS M.<br />
DOI: 10.1016/0042-6822(64)90010-8 PMID: 14165330<br />
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[3]. Redox Biol. 2021 Jan;38:101813. doi: 10.1016/j.redox.2020.101813. Epub 2020 Nov 25.<br />
Polysulfide-mediated sulfhydration of SIRT1 prevents diabetic nephropathy by suppressing phosphorylation and acetylation of p65 NF-κB and STAT3.<br />
Sun HJ(1), Xiong SP(1), Cao X(1), Cao L(1), Zhu MY(1), Wu ZY(1), Bian JS(2).<br />
Author information: (1)Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore. (2)Department of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China; Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore; National University of Singapore (Suzhou) Research Institute, Suzhou, Jiangsu, 215000, China. Electronic address: [email protected].<br />
Diabetic kidney disease is known as a major cause of chronic kidney disease and end stage renal disease. Polysulfides, a class of chemical agents with a chain of sulfur atoms, are found to confer renal protective effects in acute kidney injury. However, whether a polysulfide donor, sodium tetrasulfide (Na2S4), confers protective effects against diabetic nephropathy remains unclear. Our results showed that Na2S4 treatment ameliorated renal dysfunctional and histological damage in diabetic kidneys through inhibiting the overproduction of inflammation cytokine and reactive oxygen species (ROS), as well as attenuating renal fibrosis and renal cell apoptosis. Additionally, the upregulated phosphorylation and acetylation levels of p65 nuclear factor κB (p65 NF-κB) and signal transducer and activator of transcription 3 (STAT3) in diabetic nephropathy were abrogated by Na2S4 in a sirtuin-1 (SIRT1)-dependent manner. In renal tubular epithelial cells, Na2S4 directly sulfhydrated SIRT1 at two conserved CXXC domains (Cys371/374; Cys395/398), then induced dephosphorylation and deacetylation of its targeted proteins including p65 NF-κB and STAT3, thereby reducing high glucose (HG)-caused oxidative stress, cell apoptosis, inflammation response and epithelial-to-mesenchymal transition (EMT) progression. Most importantly, inactivation of SIRT1 by a specific inhibitor EX-527, small interfering RNA (siRNA), a de-sulfhydration reagent dithiothreitol (DTT), or mutation of Cys371/374 and Cys395/398 sites at SIRT1 abolished the protective effects of Na2S4 on diabetic kidney insulting. These results reveal that polysulfides may attenuate diabetic renal lesions via inactivation of p65 NF-κB and STAT3 phosphorylation/acetylation through sulfhydrating SIRT1.<br />
DOI: 10.1016/j.redox.2020.101813 PMCID: PMC7718489 PMID: 33279869<br />
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[4]. Int J Mol Sci. 2020 Oct 21;21(20):7805. doi: 10.3390/ijms21207805.<br />
Polysulfide and Hydrogen Sulfide Ameliorate Cisplatin-Induced Nephrotoxicity and Renal Inflammation through Persulfidating STAT3 and IKKβ.<br />
Sun HJ(1), Leng B(1), Wu ZY(1), Bian JS(1)(2).<br />
Author information: (1)Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. (2)National University of Singapore (Suzhou) Research Institute, Suzhou 215123, China.<br />
Cisplatin, a widely used chemotherapy for the treatment of various tumors, is clinically limited due to its extensive nephrotoxicity. Inflammatory response in tubular cells is a driving force for cisplatin-induced nephrotoxicity. The plant-derived agents are widely used to relieve cisplatin-induced renal dysfunction in preclinical studies. Polysulfide and hydrogen sulfide (H2S) are ubiquitously expressed in garlic, and both of them are documented as potential agents for preventing and treating inflammatory disorders. This study was designed to determine whether polysulfide and H2S could attenuate cisplatin nephrotoxicity through suppression of inflammatory factors. In renal proximal tubular cells, we found that sodium tetrasulfide (Na2S4), a polysulfide donor, and sodium hydrosulfide (NaHS) and GYY4137, two H2S donors, ameliorated cisplatin-caused renal toxicity through suppression of the massive production of inflammatory cytokines, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2). Mechanistically, the anti-inflammatory actions of Na2S4 and H2S may be mediated by persulfidation of signal transducer and activator of transcription 3 (STAT3) and inhibitor kappa B kinase β (IKKβ), followed by decreased phosphorylation of STAT3 and IKKβ. Moreover, the nuclear translocation of nuclear transcription factor kappa B (NF-κB), and phosphorylation and degradation of nuclear factor kappa B inhibitor protein alpha (IκBα) induced by cisplatin, were also mitigated by both polysulfide and H2S. In mice, after treatment with polysulfide and H2S donors, cisplatin-associated renal dysfunction was strikingly ameliorated, as evidenced by measurement of serum blood urea nitrogen (BUN) and creatinine levels, renal morphology, and the expression of renal inflammatory factors. Our present work suggests that polysulfide and H2S could afford protection against cisplatin nephrotoxicity, possibly via persulfidating STAT3 and IKKβ and inhibiting NF-κB-mediated inflammatory cascade. Our results might shed light on the potential benefits of garlic-derived polysulfide and H2S in chemotherapy-induced renal damage.<br />
DOI: 10.3390/ijms21207805 PMCID: PMC7589167 PMID: 33096924<br />
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[5]. Toxicol Lett. 2020 May 13;330:128-133. doi: 10.1016/j.toxlet.2020.05.007. Online ahead of print.<br />
Repression of mercury accumulation and adverse effects of methylmercury exposure is mediated by cystathionine γ-lyase to produce reactive sulfur species in mouse brain.<br />
Akiyama M(1), Unoki T(2), Yoshida E(3), Ding Y(4), Yamakawa H(5), Shinkai Y(1), Ishii I(6), Kumagai Y(7).<br />
Author information: (1)Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan. (2)Department of Basic Medical Sciences, National Institute for Minamata Disease, Minamata, Kumamoto 867-0008, Japan. (3)Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-0022, Japan. (4)Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Doctoral Program in Biomedical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan. (5)Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Master's Program in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan. (6)Laboratory of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan. (7)Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan. Electronic address: [email protected].<br />
Reactive sulfur species (RSS), such as hydropersulfides and hydropolysulfides with high nucleophilicity, contain mobilized sulfur that readily captures xenobiotic electrophiles, leading to their sulfur adducts. We have previously reported that RSS produced by cystathionine γ-lyase (CSE) captures the electrophilic metal methylmercury (MeHg) to form inert sulfur adducts, which in turn play a critical role in the protection against MeHg-induced motor impairment in mice. However, the mechanism underlying this neuroprotective effect is not fully understood. Here, we addressed this using CSE-knockout mice. The cerebellum of CSE-knockout mice was more susceptible to MeHg than that of wild type mice. Moreover, these CSE-deficient mice exhibited a higher level of mercury accumulation in the brain. However, co-treatment with sodium tetrasulfide, an RSS able to capture MeHg, leading to the formation of its sulfur adducts, blocked the increased accumulation of mercury, motor dysfunction and mortality caused by CSE deficiency. Our findings suggest that capturing MeHg by RSS in association with its sulfur adduct formation is involved in the repression of the brain distribution and deleterious effects of MeHg.<br />
DOI: 10.1016/j.toxlet.2020.05.007 PMID: 32413476
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