Vanadium(III)-L-cysteine protects cisplatin-induced nephropathy through activation of Nrf2/HO-1 pathway

Cisplatin (CDDP) is one of the first-line anticancer drugs; however, the major limitation of CDDP therapy is development of nephrotoxicity (25-35% cases), whose precise mechanism mainly involves oxidative stress, inflammation and cell death. Therefore, in search of a potential chemoprotectant, an or...

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Bibliographic Details
Published in:Free radical research 2016-01, Vol.50 (1), p.39-55
Main Authors: Basu, Abhishek, Singha Roy, Somnath, Bhattacharjee, Arin, Bhuniya, Avishek, Baral, Rathindranath, Biswas, Jaydip, Bhattacharya, Sudin
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - toxicity
Antioxidant
Antioxidants - metabolism
ARE pathway
Blood Urea Nitrogen
Cell Line, Tumor
chemotherapy
Cisplatin - toxicity
Coordination Complexes - chemistry
Coordination Complexes - therapeutic use
Creatinine - blood
Cysteine - analogs & derivatives
Cysteine - chemistry
Cysteine - therapeutic use
Female
free radicals
Heme Oxygenase-1 - metabolism
Humans
inflammation
Kidney Diseases - blood
Kidney Diseases - chemically induced
Kidney Diseases - drug therapy
Kidney Diseases - metabolism
Mice
NF-E2-Related Factor 2 - metabolism
Oxidative Stress - drug effects
Protective Agents - pharmacology
Signal Transduction
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Summary:Cisplatin (CDDP) is one of the first-line anticancer drugs; however, the major limitation of CDDP therapy is development of nephrotoxicity (25-35% cases), whose precise mechanism mainly involves oxidative stress, inflammation and cell death. Therefore, in search of a potential chemoprotectant, an organovanadium complex, viz., vanadium(III)-L-cysteine (VC-III) was evaluated against CDDP-induced nephropathy in mice. CDDP was administered intraperitoneally (5 mg/kg b.w.) and VC-III was given by oral gavage (1 mg/kg b.w.) in concomitant and pre-treatment schedule. The results showed that VC-III administration reduced (p 
ISSN:1071-5762
1029-2470
DOI:10.3109/10715762.2015.1102908