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Prevention of cisplatin-induced nephrotoxicity by glucosides of ascorbic acid and alpha-tocopherol.
Exp Toxicol Pathol. 2008 Sep; 60(6):521-7.ET

Abstract

BACKGROUND

Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses, causes many physiological adverse effects such as nephrotoxicity and genotoxicity. The toxicity of the drug has been attributed to the induction of oxidative free radicals.

METHODS

Following intraperitoneal administration of cisplatin and ascorbic acid monoglucoside (AsAG) or alpha-tocopherol monoglucoside (TMG), investigations were conducted on levels of serum urea and creatinine, peroxidation of lipids in renal tissues, renal antioxidants and histopathology of renal tissue.

RESULTS

Administration of cisplatin to mice induced a marked renal failure, characterized by significant increase in serum urea and creatinine levels in addition to severe alterations in renal tissue architecture. Cisplatin also induced oxidative stress as indicated by increased lipid peroxidation and decreased levels of reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase in renal tissues. Administration of AsAG or TMG markedly reduced the cisplatin-induced higher plasma creatinine and urea levels and counteracted the deleterious effects of cisplatin on oxidative stress markers and protected the tissues from the cisplatin-induced lipid peroxidation.

CONCLUSION

These results indicated that AsAG or TMG has a protective effect against cisplatin-induced renal damage in mice. The protection is mediated by preventing the decline of antioxidant status. The results have implications in use of AsAG or TMG in human application for protecting against drug-induced nephrotoxicity.

Authors+Show Affiliations

Amala Cancer Research Centre, Trichur 680555, Kerala, India.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18644706

Citation

Maliakel, Dani Mathew, et al. "Prevention of Cisplatin-induced Nephrotoxicity By Glucosides of Ascorbic Acid and Alpha-tocopherol." Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie, vol. 60, no. 6, 2008, pp. 521-7.
Maliakel DM, Kagiya TV, Nair CK. Prevention of cisplatin-induced nephrotoxicity by glucosides of ascorbic acid and alpha-tocopherol. Exp Toxicol Pathol. 2008;60(6):521-7.
Maliakel, D. M., Kagiya, T. V., & Nair, C. K. (2008). Prevention of cisplatin-induced nephrotoxicity by glucosides of ascorbic acid and alpha-tocopherol. Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie, 60(6), 521-7. https://doi.org/10.1016/j.etp.2008.04.015
Maliakel DM, Kagiya TV, Nair CK. Prevention of Cisplatin-induced Nephrotoxicity By Glucosides of Ascorbic Acid and Alpha-tocopherol. Exp Toxicol Pathol. 2008;60(6):521-7. PubMed PMID: 18644706.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prevention of cisplatin-induced nephrotoxicity by glucosides of ascorbic acid and alpha-tocopherol. AU - Maliakel,Dani Mathew, AU - Kagiya,Tsutomu V, AU - Nair,Cherupally Krishnan Krishnan, Y1 - 2008/07/21/ PY - 2008/03/17/received PY - 2008/04/21/revised PY - 2008/04/22/accepted PY - 2008/7/23/pubmed PY - 2008/10/24/medline PY - 2008/7/23/entrez SP - 521 EP - 7 JF - Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie JO - Exp Toxicol Pathol VL - 60 IS - 6 N2 - BACKGROUND: Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses, causes many physiological adverse effects such as nephrotoxicity and genotoxicity. The toxicity of the drug has been attributed to the induction of oxidative free radicals. METHODS: Following intraperitoneal administration of cisplatin and ascorbic acid monoglucoside (AsAG) or alpha-tocopherol monoglucoside (TMG), investigations were conducted on levels of serum urea and creatinine, peroxidation of lipids in renal tissues, renal antioxidants and histopathology of renal tissue. RESULTS: Administration of cisplatin to mice induced a marked renal failure, characterized by significant increase in serum urea and creatinine levels in addition to severe alterations in renal tissue architecture. Cisplatin also induced oxidative stress as indicated by increased lipid peroxidation and decreased levels of reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase in renal tissues. Administration of AsAG or TMG markedly reduced the cisplatin-induced higher plasma creatinine and urea levels and counteracted the deleterious effects of cisplatin on oxidative stress markers and protected the tissues from the cisplatin-induced lipid peroxidation. CONCLUSION: These results indicated that AsAG or TMG has a protective effect against cisplatin-induced renal damage in mice. The protection is mediated by preventing the decline of antioxidant status. The results have implications in use of AsAG or TMG in human application for protecting against drug-induced nephrotoxicity. SN - 0940-2993 UR - https://www.unboundmedicine.com/medline/citation/18644706/Prevention_of_cisplatin_induced_nephrotoxicity_by_glucosides_of_ascorbic_acid_and_alpha_tocopherol_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0940-2993(08)00088-2 DB - PRIME DP - Unbound Medicine ER -