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}
}
  • D. Dickey, Y. J. Wu, E. Neuwelt
  • Published 1 September 2005
  • Biology, Medicine
  • Journal of Pharmacology and Experimental Therapeutics
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
TLDR
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
TLDR
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.
Ameliorating effect of DL-α-lipoic acid against cisplatin-induced nephrotoxicity and cardiotoxicity in experimental animals.
TLDR
LA is suggested to be a potential candidate to ameliorate cisplatin-induced nephrotoxicity and cardiotoxicity without altering the antitumor efficacy of cis platin.
Abrogation of cisplatin-induced nephrotoxicity in mice by alpha lipoic acid through ameliorating oxidative stress and enhancing gene expression of antioxidant enzymes.
N-acetylcysteine chemoprotection without decreased cisplatin antitumor efficacy in pediatric tumor models
TLDR
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
TLDR
It is suggested that oxidative stress and inflammation are involved in the pathogenesis of CP-induced acute renal failure and the inhibition of the inflammatory biomarkers by NAC or TAU after CP administration may play a central role in modulation of nephrotoxicity induced by CP.
The ameliorative effect of cysteine prodrug l‐2‐oxothiazolidine‐4‐carboxylic acid on cisplatin‐induced nephrotoxicity in rats
TLDR
The results suggested that OTC had ameliorated the histopathological and biochemical indices of nephrotoxicity in rats, and may potentially be useful as a nephroprotective agent.
Protective effect of l-carnitine versus amifostine against cisplatin-induced nephrotoxicity in rats
TLDR
It is suggested that application of AMF before CDDP may enhance CDDP-induced nephrotoxicity histopathologically and not have a protective effect on AMF or CAR.
Sodium Thiosulfate Administered Six Hours after Cisplatin Does Not Compromise Antineuroblastoma Activity
TLDR
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.
TLDR
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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