Cancer anti-carcinogenic activity

Finally, susceptibility to cancer may be increased by an inadequate intake of biologically active food components, which, though not classified as nutrients, may nevertheless exert important anti-carcinogenic effects over... 

In addition to effects on body composition, CLA has been investigated extensively for its inhibiting effects on cancer. A number of studies have reported a moderate inhibitory effect of CLA on the growth of several human tumor cell lines such as breast cancer cells (38), colon cancer cells (39), lung adenocarcinoma cells (40), prostate cancer cells (41), and melanoma (skin) cells (42). In in vivo studies in mostly rats and mice, CLA has shown anti-carcinogenic properties as well. Both anti-initiation activity and inhibitory effects on tumor promotion by CLA have been reported. The work by Ip et al. clearly demonstrated an anti-carcinogenic effect of CLA on mammary tumors in... 

Many claims for health benefits have been made for CLA in both animals and humans. These have been reviewed in detail elsewhere (Yurawecz et al, 1999a) and will only be discussed briefly here. The first indication that CLA might be biologically active was reported in 1979 when an extract from grilled beef was found to inhibit mutagenesis in a rat liver cell fraction (Pariza et al, 1979). Studies on the potentially anti-carcinogenic properties of CLA, both in vitro and in vivo (Pariza et al, 2001), have demonstrated that the isomer with an active effect on cancer cells is probably the 9-cis, ll-trans isomer. In vivo studies in rodents showed that dietary CLA supplementation decreased the number and size of mammary tumours, regardless of other lipid intake (Ip et al, 1996), and that topically applied CLA reduced the size and number of skin... 

DFBcPh and its dihydrodiol were subjected to metabolism, and the extent of DNA binding in human breast cancer MCF-7 cells was assessed." The extent of DNA binding was then compared with that for BcPh and its dihydrodiol and the potent carcinogen BaP. The 1,4-DFBcPh series 2 (anti) DE-derived DNA adducts were also compared with those arising from intracellular oxidation of the dihydrodiol with subsequent DNA binding. These experiments showed that increased molecular distortion decreased metabolic activation to the terminal metabolites but the DE metabolites formed were the DNA-damaging species. 

DATS which are potent inhibitors of BP-induced fore-stomach cancer in mice, resulted in a significant increase, as compared with control, in bodi hepatic (3.0-, 3.2-and 4.4-fold, respectively) and fore-stomach (1.5-, 2.7-and 2.7-fold, respectively) glutathione transferase (GST) activity toward anti-7P,8a-dihy oxy-9a, 1 Oa-oxy-7,8,9,10-tetrahydrobenzo(a)pyrene (anti-BPDE), which is the ultimate carcinogen of BP [102, 107]. On the contrary, this activity was not increased in either organ by dipropyl sulfide (DPS), which is ineffective against BP-induced fore-stomach cancer. The pulmonary GST activity was not increased by any of the tested OSCs. Even though epoxide hydrolase (EH) activity was differentially altered by these OSCs, a correlation between chemopreventive efficacy of OSCs and their effects on EH activity was not apparent [102]. The chemopreventive efficacy of these OSCs correlated with their ability to increase the expression of GST n. For example, DAS treatment resulted in approximate increases of 1.7- and 2.2-fold in hepatic and fore-stomach GST n expression, respectively, over the control. Treatment of mice with DATS, which is a relatively more potent inhibitor of BP-induced fore-stomach cancer than DAS, resulted in about 3.8- and 3,2-fold increases, respectively, in hepatic and fore-stomach GST n expression over the control. On the contrary, the expression of hepatic and fore-stomach GST n was increased only marginally (10-20%) upon DPS administration [107],... 

The disturbances in protein phosphorylation patterns in Cr(VI) treated cells are considered among the possible reasons for Cr(VI) toxicity and carcinogenicity (295, 626). The question then arises, as to whether the proposed beneficial action of Cr(III) in activation of insulin receptor tyrosine kinase (496,497) is, in fact, a sign of Cr(III) toxicity (5). Unpredictable changes in the concentrations of phosphorylated proteins in the presence of excess Cr(III) may lead to abnormalities in the cell signaling pathways and ultimately to cancer (5). An answer to this dilemma may lie in selectivity studies (which are yet to be performed) of different types of Cr(III) complexes toward various kinases or phosphatases. Clearly, the Cr(III) complexes of potential use as anti-diabetics should be highly selective in the activation of protein tyrosine kinase of the p-subunit of the insulin receptor (496, 497). On the other hand, the potential ability of some Cr(III) complexes to selectively activate non-insulin dependent protein kinases may lead to beneficial effects, such as stimulation of immune responses or antitumor activity (627, 628). 

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