ABSTRACT
The effect of a pungent ingredient of red pepper, capsaicin, on oxidative stress induced changes in the antioxidant defense system by benzo(a)pyrene in the lungs of mice was studied. Oral gavage administration of benzo(a)pyrene (50 mg/kg body weight) to mice led to a marked increase in oxidative stress indicated by alterations in pulmonary lipid peroxidation, enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase) and non-enzymic antioxidants (reduced glutathione, vitamin C, vitamin E and vitamin A). Pre-co-treatment with capsaicin (10 mg/kg body weight i.p.) restored cellular normalcy, highlighting the antioxidant potential of capsaicin in mitigating the oxidative stress mediated damage produced during benzo(a)pyrene-induced lung cancer.
Subject(s)
Antioxidants/metabolism , Capsaicin/pharmacology , Lung Neoplasms/prevention & control , Lung/drug effects , Animals , Ascorbic Acid/metabolism , Benzo(a)pyrene , Catalase/metabolism , Glucosephosphate Dehydrogenase/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Glutathione Transferase/metabolism , Lipid Peroxidation/drug effects , Lung/metabolism , Lung/pathology , Lung Neoplasms/chemically induced , Lung Neoplasms/metabolism , Male , Mice , Oxidative Stress/drug effects , Superoxide Dismutase , Vitamin A/metabolism , Vitamin E/metabolismABSTRACT
The modulatory efficacy of capsaicin on lung mitochondrial enzyme system with reference to mitochondrial lipid peroxidation (LPO), antioxidants, key citric acid cycle enzymes and respiratory chain enzymes during benzo(a)pyrene (B(a)P) induced lung cancer in Swiss albino mice was studied. Elevations in mitochondrial LPO along with decrements in enzymic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)), non-enzymic antioxidants (reduced glutathione (GSH), vitamin C, vitamin E and vitamin A), citric acid cycle enzymes (isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (alpha-KDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH)), and respiratory chain enzymes (NADH dehydrogenase and Cytochrome c oxidase) were observed in B(a)P (50mg/kg body weight) administered animals. CAP (10mg/kg body weight) pretreatment decreased lung mitochondrial LPO and augmented the activities of enzymic, non-enzymic antioxidants, citric acid cycle enzymes and respiratory chain enzymes to near normalcy revealing its chemoprotective function during B(a)P induced lung cancer.
Subject(s)
Anticarcinogenic Agents/pharmacology , Antioxidants/metabolism , Capsaicin/pharmacology , Lung Neoplasms/prevention & control , Animals , Benzo(a)pyrene/toxicity , Enzymes/drug effects , Enzymes/metabolism , Lipid Peroxidation/drug effects , Lung Neoplasms/chemically induced , Male , Mice , Mitochondria/drug effects , Mitochondria/metabolism , Neoplasms, Experimental/chemically induced , Neoplasms, Experimental/prevention & controlABSTRACT
AIM: To study the effect of silymarin on the levels of tumor markers and MDA (malondialdehyde)-DNA adduct formation during N-nitrosodiethylamine induced hepatocellular carcinoma in male Wistar albino rats. METHODS: The levels of AFP, CEA and activities of liver marker enzymes in serum, MDA-DNA immunohistochemistry were done according to standard procedures in the control and experimental groups of rats. RESULTS: Hepatocellular carcinoma was evidenced from significant (p < 0.05) increases of alpha-fetoprotein, carcinoembryonic antigen, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase, lactate dehydrogenase, gamma-glutamyltransferase and 5'-nucleotidase in serum and increased MDA-DNA adducts were also observed in the tissue sections of hepatocellular carcinoma. Silymarin treatment significantly attenuated the alteration of these markers and decreased the levels of MDA-DNA adduct formation. CONCLUSION: Silymarin could be developed as a promising chemotherapeutic adjuvant for the treatment of liver cancer.
