title: Catechin prevents tamoxifen-induced oxidative stress and biochemical perturbations in mice.
abstract: Natural antioxidants like catechin are now known to have a modulatory role on physiological functions and biotransformation reactions involved in the detoxification process, thereby affording protection from toxic metabolic actions of xenobiotics. Reactive oxygen intermediates have been demonstrated to play an etiological role in anticancer drug-induced toxicity. This study was performed to explore the modulatory and protective effect of catechin on the toxicity of an anticancer drug, tamoxifen (TAM) with special reference to protection against disruption of glutathione metabolizing and antioxidant enzymes. TAM treatment resulted in a significant increase in the lipid peroxidation (LPO), H(2)O(2) generation and protein carbonyl (PC) contents in the liver and kidney as compared to controls while catechin+TAM-treated group showed significant decrease in LPO levels, H(2)O(2) generation and PC contents in liver and kidney when compared with TAM-treated group. Non-enzymatic antioxidants like reduced glutathione (GSH) and low molecular antioxidants like ascorbic acid (AsA) also showed normalcy due to exogenous catechin administration. Catechin pre-treatment showed restoration in the level of cytochrome P450 (CYP) content and in the activities of glutathione metabolizing enzymes, viz., glutathione-S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx) and other antioxidant enzymes such as, glucose-6-phosphate dehydrogenase (G6-PD), catalase (CAT) and superoxide dismutase (SOD) in both liver and kidney when compared to TAM-treated animals. The results of the study show that catechin supplementation might be helpful in abrogation of TAM toxicity during chemotherapy. Additionally, it makes it a prophylactic and preventive agent of anticancer drug-induced oxidative stress.
authors.affiliation: Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India. drsuhelparvez@yahoo.com
authors.forename: Suhel
authors.initials: S
authors.lastname: Parvez
authors.forename: Heena
authors.initials: H
authors.lastname: Tabassum
authors.forename: Hasibur
authors.initials: H
authors.lastname: Rehman
authors.forename: Basu Dev
authors.initials: BD
authors.lastname: Banerjee
authors.forename: Mohammad
authors.initials: M
authors.lastname: Athar
authors.forename: Sheikh
authors.initials: S
authors.lastname: Raisuddin
mesh_terms: D000818:Animals; D018931:Antineoplastic Agents, Hormonal / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000378:metabolism; D002392:Catechin / Q000494:pharmacology*; D004336:Drug Antagonism; D004359:Drug Therapy, Combination; D004798:Enzymes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation / Q000187:drug effects; D013629:Tamoxifen / Q000633:toxicity*
chemical_list: D018931:Antineoplastic Agents, Hormonal; D000975:Antioxidants; D004798:Enzymes; D013629:Tamoxifen; D002392:Catechin; D006861:Hydrogen Peroxide; D005978:Glutathione; D001205:Ascorbic Acid