ABSTRACT
Lung cancer is one of the leading causes of cancer death in the world and is notoriously difficult to treat effectively. In the present study, male Swiss albino mice were divided into five groups of six animals each: group I animals received corn oil orally and served as a control; group II cancer-induced animals received benzo(a)pyrene (B[a]P) (50 mg kg(-1) bodyweight dissolved in corn oil, orally) twice weekly for four successive weeks; group III cancer-bearing animals (after 12 weeks of induction) were treated with cisplatin (6 mg kg(-1) bodyweight, i.p.) once weekly for 4 weeks; group IV cancer-bearing animals were treated with cisplatin along with Solanum trilobatum (300 mg kg(-1) bodyweight) orally once weekly for 4 weeks; and group V animals constituted the drug control treated with cisplatin along with S. trilobatum. The serum, lung and liver were investigated biochemically for aryl hydrocarbon hydroxylase, gamma-glutamyl transpeptidase, 5'-nucleotidase, lactate dehydrogenase (LDH) and protein-bound carbohydrate components (hexose, hexosamine and sialic acid). These enzyme activities were increased significantly in cancer-bearing animals compared with control animals. The elevation of these in cancer-bearing animals was indicative of the persistent deteriorating effect of B[a]P in cancer-bearing animals. Our data suggest that cisplatin, administered with S. trilobatum, may extend its chemotherapeutic effect through modulating protein-bound carbohydrate levels and marker enzymes, as they are indicators of cancer. The combination of cisplatin with S. trilobatum could effectively treat the B[a]P-induced lung cancer in mice by offering protection from reactive oxygen species damage and also by suppressing cell proliferation.
Subject(s)
Antineoplastic Agents/therapeutic use , Benzo(a)pyrene/toxicity , Cisplatin/therapeutic use , Lung Neoplasms/drug therapy , Plant Extracts/therapeutic use , Solanum/chemistry , Animals , Antineoplastic Agents/administration & dosage , Cisplatin/administration & dosage , Lung Neoplasms/chemically induced , Male , Mice , Plant Extracts/administration & dosageABSTRACT
The present study is an effort to identify a potent chemopreventive agent against cancer, in which oxidative stress plays an important causative role. The modulatory effect of mangiferin on mitochondrial lipid peroxidation (LPO), tricarboxylic acid (TCA) cycle key enzymes and electron transport chain complexes was investigated against lung carcinogenesis induced by benzo(a)pyrene (50 mg kg(-1) b/w orally) in Swiss albino mice. Decreased activities of electron transport chain complexes and TCA cycle key enzymes such as isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH), in lung cancer bearing animals were observed. Pre- and post-treatment with mangiferin (100 mg kg(-1) b/w orally) for 18 weeks, prevented the above biochemical changes, which were inclined towards normal control animal values. This study further confirms the chemopreventive and chemotherapeutic effect of mangiferin and these results are consistent with our hypothesis that mangiferin is a promising chemopreventive agent.