Preparation and antioxidant properties of extracts of Japanese persimmon leaf tea (kakinoha-cha)

Phenolic contents and antioxidant activities of bitter gourd (Momordica charantia L.) leaf, stem and fruit fraction extracts in vitro.

Antioxidant and free radical-scavenging activities of smooth hound (Mustelus mustelus) muscle protein hydrolysates obtained by gastrointestinal proteases

Despite significant advances in medicine, liver cancer, predominantly hepatocellular carcinoma remains a major cause of death in the United States as well as the rest of the world. As limited treatment options are currently available to patients with liver cancer, novel preventive control and effective therapeutic approaches are considered to be reasonable and decisive measures to combat this disease. Several naturally occurring dietary and non-dietary phytochemicals have shown enormous potential in the prevention and treatment of several cancers, especially those of the gastrointestinal tract. Terpenoids, the largest group of phytochemicals, traditionally used for medicinal purposes in India and China, are currently being explored as anticancer agents in clinical trials. Terpenoids (also called “isoprenoids”) are secondary metabolites occurring in most organisms, particularly plants. More than 40 000 individual terpenoids are known to exist in nature with new compounds being discovered every year. A large number of terpenoids exhibit cytotoxicity against a variety of tumor cells and cancer preventive as well as anticancer efficacy in preclinical animal models. This review critically examines the potential role of naturally occurring terpenoids, from diverse origins, in the chemoprevention and treatment of liver tumors. Both in vitro and in vivo effects of these agents and related cellular and molecular mechanisms are highlighted. Potential challenges and future directions involved in the advancement of these promising natural compounds in the chemoprevention and therapy of human liver cancer are also discussed.

Terpenoids as potential chemopreventive and therapeutic agents in liver cancer.

Evaluation of antioxidant activity of parsley (Petroselinum crispum) essential oil and identification of its antioxidant constituents

The anti-cancer efficacy of dietary beta-carotene (BC, 120 mg/kg diet, daily) was evaluated during diethylnitrosamine (DEN, 200 mg/kg body weight)-induced hepatocarcinogenesis in male Sprague-Dawley rats. BC treatment was carried out throughout the study, before initiation or selection/promotion phase of hepatocarcinogenesis in a defined experimental protocol. In red blood cells (RBC) and microsomal fractions from hepatic nodular and non-nodular surrounding parenchyma, the enzymatic lipid peroxidation increased significantly by more than 3-fold, 9- to 10-fold and 4- to 7-fold respectively 18 weeks following initiation by DEN as compared to normal control animals. RBC membrane protein damage was estimated by alanine release and was found to increase more than 5-fold in the same time period in DEN control rats. A decrease in hepatic cytosolic and microsomal glucose-6-phosphatase activities was observed, whereas the activities of the oxygen-derived free-radical scavenger enzymes, like cytosolic catalase and superoxide dismutase, were shown to increase significantly at the same time point. However, BC exposure in the different phases to hepatocarcinogenesis substantially changed all the above parameters in limiting the action of DEN. Results showed that the most significant beneficial effect of BC during hepatocarcinogenesis was exerted mainly in long term continuous and/or the initiation phase of carcinogenicity, rather than in the selection/promotion phase. Moreover, the volumetric and numerical densities of the preneoplastic lesions were all appreciably reduced by exposure to BC. We conclude that long term intake of BC could reduce cancer risk by preventing hepatic lipid peroxidation and RBC membrane protein damage due to its antioxidant actions.

A. Bishayee

Papers

Beta-carotene prevents lipid peroxidation and red blood cell membrane protein damage in experimental hepatocarcinogenesis