Protection against Cisplatin-Induced Toxicities by N-Acetylcysteine and Sodium Thiosulfate as Assessed at the Molecular, Cellular, and in Vivo Levels
@article{Dickey2005ProtectionAC, title={Protection against Cisplatin-Induced Toxicities by N-Acetylcysteine and Sodium Thiosulfate as Assessed at the Molecular, Cellular, and in Vivo Levels}, author={D. Thomas Dickey and Y J Wu and Leslie L. Muldoon and Edward A. Neuwelt}, journal={Journal of Pharmacology and Experimental Therapeutics}, year={2005}, volume={314}, pages={1052 - 1058} }
Cisplatin (CDDP) is a common, highly toxic chemotherapeutic agent. This study investigates chemoprotective effects of N-acetylcysteine (NAC) and sodium thiosulfate (STS) on in vitro and in vivo CDDP toxicities. For ototoxicity studies, CDDP (6 mg/kg) was administered to rats via a retrograde carotid artery infusion. Auditory brainstem response thresholds at 4 to 20 kHz were tested before and 7 days post-treatment. STS (8 g/m2 i.v.) was administered at 4, 8, or 12 h after CDDP. For…
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Effect of N-acetylcysteine route of administration on chemoprotection against cisplatin-induced toxicity in rat models
- Medicine, BiologyCancer Chemotherapy and Pharmacology
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The protective properties of NAC are affected by the dose and route of administration, and blood concentrations of total NAC showed a dose response after IV NAC, but high dose NAC (1,200 mg/kg) by the PO route gave very low levels of Nac.
Role of N-Acetylcystein in Protection against Cisplatin Nephrotoxicity
- Biology, Medicine
- 2010
NAC protection is mediated by preventing the decline of antioxidant status, inhibit malondialdehyde and TNF-α and prevent necrosis and apoptosis from kidneys and have implications in use of NAC in human application for protecting against drug-induced nephrotoxicity.
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- Biology, ChemistryDrug discoveries & therapeutics
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LA is suggested to be a potential candidate to ameliorate cisplatin-induced nephrotoxicity and cardiotoxicity without altering the antitumor efficacy of cis platin.
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- BiologyEuropean journal of pharmacology
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- Medicine, BiologyJournal of Neuro-Oncology
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Data support a Phase I/II clinical trial of delayed NAC to reduce ototoxicity in children with localized pediatric cancers and support a minimally nephrotoxic cisplatin therapy if delayed until 4 h after chemotherapy.
Possible mechanisms for N-acetyl cysteine and taurine in ameliorating acute renal failure induced by cisplatin in rats
- Biology, MedicineToxicology mechanisms and methods
- 2011
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- Biology, ChemistryFundamental & clinical pharmacology
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- Medicine, BiologyMedical oncology
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- Biology, MedicineClinical Cancer Research
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Preclinical data suggest that the use of STS 6 h after cisplatin for otoprotection is unlikely to compromise the antineuroblastoma activity of cisPlatin.
The molecular mechanisms of the attenuation of cisplatin-induced acute renal failure by N-acetylcysteine in rats.
- Biology, MedicineNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
- 2008
Data suggest that oxidative stress and p38 MAPK-mediated apoptotic cell death pathways are involved, at least in part, in the pathogenesis of CDDP-induced ARF, and negative regulation of p38MAPK activation through inhibition of oxidative stress appears to play a central role in the beneficial effects of NAC.
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