Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms20020313
Title: Protective smell of hydrogen sulfide and polysulfide in cisplatin-induced nephrotoxicity
Authors: Cao X. 
Zhang W.
Moore P.K. 
Bian J. 
Keywords: 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene
2 (2 amino 3 methoxyphenyl)chromone
acetylcysteine
carrier proteins and binding proteins
cisplatin
copper transporter
cystathionine gamma lyase
cysteine
cytochrome P450
cytochrome P450 2E1
cytokine
homocysteine
hydrogen polysulfide
hydrogen sulfide
interleukin 10
interleukin 18
interleukin 1beta
interleukin 2
messenger RNA
mitogen activated protein kinase
mitogen activated protein kinase kinase 1
monocyte chemotactic protein 1
organic cation transporter 2
reactive oxygen metabolite
reduced nicotinamide adenine dinucleotide phosphate oxidase
stress activated protein kinase
sulfide
synaptophysin
tumor necrosis factor
unclassified drug
cystathionine gamma lyase
GYY 4137
hydrogen sulfide
morpholine derivative
phosphorothioic acid derivative
reactive oxygen metabolite
antiapoptotic activity
antineoplastic activity
antioxidant activity
biosynthesis
cell death
clinical trial (topic)
dimerization
down regulation
drug accumulation
enzyme activity
enzyme inhibition
human
hydrogen sulfide biosynthesis
inflammation
kidney microsome
MAPK signaling
molecular mechanics
nephrotoxicity
nonhuman
oxidative stress
pathophysiology
protein expression
renal protection
Review
risk factor
signal transduction
therapy effect
chemically induced
complication
drug effect
gene expression regulation
genetics
kidney
kidney disease
metabolism
neoplasm
odor
oxidation reduction reaction
pathology
Cisplatin
Cystathionine gamma-Lyase
Gene Expression Regulation, Neoplastic
Humans
Hydrogen Sulfide
Kidney
Kidney Diseases
Morpholines
Neoplasms
Organothiophosphorus Compounds
Oxidation-Reduction
Reactive Oxygen Species
Smell
Issue Date: 2019
Citation: Cao X., Zhang W., Moore P.K., Bian J. (2019). Protective smell of hydrogen sulfide and polysulfide in cisplatin-induced nephrotoxicity. International Journal of Molecular Sciences 20 (2) : 313. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms20020313
Abstract: Though historically known as a toxic gas, hydrogen sulfide (H 2 S) has displayed a new face as the third endogenous gaseous signaling molecule after nitric oxide (NO) and carbon monoxide (CO). Here in this review, we survey the role and therapeutic potential of H 2 S in cisplatin-induced nephrotoxicity. Specifically, reduction of H 2 S by cystathionine γ-lyase (CSE) downregulation upon cisplatin treatment may contribute to cisplatin-induced renal cell injury, possibly by augmentation of endogenous reactive oxygen species (ROS) production, while H 2 S donation may prevent subsequent renal dysfunction by inhibiting NADPH oxidase activation. Intriguingly, H 2 S slow-releasing compound GYY4137 seems to increase the anticancer activity of cisplatin, at least in several cancer cell lines, and this is probably due to its own anticancer effect. However, the efficacy of H 2 S donors in tumor-bearing animals remains to be tested in terms of renal protection and cancer inhibition after receiving cisplatin. Furthermore, accumulative evidence regarding usage of polysulfide, a novel H 2 S derived molecule, in the therapy of cisplatin-induced nephrotoxicity, was also summarized. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Source Title: International Journal of Molecular Sciences
URI: https://scholarbank.nus.edu.sg/handle/10635/174660
ISSN: 1661-6596
DOI: 10.3390/ijms20020313
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