s-Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity

  title={s-Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity},
  author={H L Kuo and Mei-chin Mong and Hung-Chih Chen and Zhi‐hong Wang and Mei-chin Yin},
  journal={Amino Acids},
  pages={1181 - 1190}
Renal protection from s-ethyl cysteine (SEC) against cisplatin (CP)-induced inflammatory and oxidative injury was examined. Mice were divided into five groups: normal group, 0.25% SEC group, CP group, 0.125% SEC + CP group, 0.25% SEC + CP group. After 2 weeks supplementation, mice of CP and SEC + CP groups received CP treatment. H&E stain showed that CP caused infiltration of inflammatory cells and necrosis of tubular cells. SEC pre-treatments attenuated CP-induced inflammatory injury and… 

Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NAD+-Dependent Enzymes and Plant-Derived Natural Products

The underlying mechanisms of cisplatin kidney injury are reviewed in the context of NAD+-dependent redox enzymes including mitochondrial complex I, NAD kinase, CD38, sirtuins, poly-ADP ribosylase polymerase, and nicotinamide nucleotide transhydrogenase and their potential contributing roles in the amelioration of cisPlatin-induced kidney injury conferred by natural products derived from plants.



Protective and alleviative effects from 4 cysteine-containing compounds on ethanol-induced acute liver injury through suppression of oxidation and inflammation.

Results support that SEC and SPC could provide both preventive and alleviative effects against alcohol-induced hepatotoxicity through suppression of oxidation and inflammation.

Amelioration of cisplatin nephrotoxicity by genetic or pharmacologic blockade of prostaglandin synthesis.

Results suggest the activation of COX-2/mPGES-1 pathway in renal parenchymal cells may selectively mediate cisplatin-induced renal injury and offer a novel therapeutic target for management of the adverse effect of cisPlatin chemotherapy.

Five cysteine-containing compounds delay diabetic deterioration in Balb/cA mice.

via their antioxidant activities, the 5 compounds effectively improved glycemic control, delayed oxidation damage, downregulated inflammatory cytokines, and enhanced anticoagulant activity in diabetic mice, and support the multiple roles of these agents as potential protective agents for delaying diabetic deterioration.

Sinapic acid modulates Nrf2/HO-1 signaling pathway in cisplatin-induced nephrotoxicity in rats.

  • M. Ansari
  • Biology, Chemistry
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
  • 2017

Antiinflammatory and antifibrogenic effects of s-ethyl cysteine and s-methyl cysteine in the kidney of diabetic mice.

Results showed that the intake of SEC or SMC alleviated body weight loss and urine output, as well as markedly decreased plasma blood urea nitrogen and creatinine clearance in diabetic mice, and the supplement might be helpful for the prevention or treatment of diabetic kidney diseases.

Melatonin suppresses cisplatin-induced nephrotoxicity via activation of Nrf-2/HO-1 pathway

Melatonin attenuates cisplatin-induced nephrotoxicity possibly by modulating Nrf2/HO-1 signaling, and this study suggests that the mechanism of the protective effect of melatonin against cisplarin-induced renal damage is still essentially unknown.

Antiglycative and anti-VEGF effects of s-ethyl cysteine and s-propyl cysteine in kidney of diabetic mice.

The present study suggests the supplement of SEC or SPC might be helpful for the prevention or treatment of diabetic kidney diseases via alleviating renal glycative injury.

Role of oxidative and nitrosative stress in cisplatin-induced nephrotoxicity.

  • Y. ChirinoJ. Pedraza-Chaverri
  • Biology
    Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie
  • 2009