Peptides remaining or appearing during protein digestion were examined for a possibility of their involvement in the regulation of cholesterol levels in plasma. Plant proteins were somewhat inferior in digestibility to casein and their digestive products were abundant in 'hydrophobic' peptides relative to casein. The 'hydrophobic' peptides bound well to bile acid. There was a correlation between the plasma cholesterol level in rats given various food proteins and the hydrophobicity of their digestive products (peptic-pancreatic digests).

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Mouse ileal sodium dependent bile acid transporter (ISBT) was characterized using isolated enterocytes. Only enterocytes from the most distal portion showed Na+-dependent [3H]taurocholate uptake. Northern blot analysis using a probe against mouse ISBT revealed the expression of mouse ISBT mRNA to be restricted to the distal ileum. The Km and Vmax for Na+-dependent [3H]taurocholate transport into isolated ileocytes were calculated as 27 microM and 360 pmol/mg protein/min, respectively. Uptake of [3H]taurocholate was inhibited by N-ethylmaleimide. We have cloned ISBT cDNA from mouse ileum. The cDNA included the entire open reading frame coding 348 amino acid protein with seven hydrophobic segments and two N-glycosylation sites. COS-7 cells transfected with the expression vector containing this cDNA expressed Na+-dependent [3H]taurocholate uptake activity with a Km of 34 microM.

Various proteins were examined for their antioxidant effects in powder model systems. Wheat gliadin that was prepared from gluten by extraction with 70% ethanol, but not gluten and its component "glutenin", was the most effective in antioxidation against linoleate peroxidation under the experimental conditions (40 °C, Aw = 0.6). Maize zein, ovalbumin, and soy protein isolate followed it to a lesser extent. The antioxidant effect of gliadin was found closely correlated with the moisture in the model system. At a high Aw, the peroxide value was maintained at a marginal level during storage. A quite similar tendency was observed for residual linoleic acid determined by gas chromatography; the ratio of linoleic acid to palmitic acid (an internal standard) remained unchangeable throughout the experimental period.Polyunsaturated fatty acids (PUFA) such as linoleic,

Hydrophobic bile acids induce apoptosis in both colon cancer cells and hepatocytes. The mechanism by which colon cancer cells respond to bile acids is thought to be different from that of hepatocytes. Therefore, we investigated the characteristics of apoptosis in colon cancer cell line HCT116. Hydrophobic bile acids, i.e., deoxycholic acid (DCA), and chenodeoxycholic acid, induced apoptosis in HCT116 cells. Apoptotic indications were detectable at as early as 30 min and the extent increased in time- and concentration-dependent manners. SDS and a hydrophilic bile acid, cholic acid, did not induce apoptosis even at cytotoxic concentrations. Pretreatment with cycloheximide failed to inhibit apoptosis, suggesting that protein synthesis is not involved in the apoptotic response. Release of cytochrome c from mitochondria and activation of caspase-9 were detectable after 5 and 10 min, respectively, whereas remarkable activation of Bid was not detected. Ursodeoxycholic acid (UDCA) protected HCT116 cells from DCA-induced apoptosis but a preincubation period of > or =5 h was required. Nevertheless, UDCA did not inhibit cytochrome c release from mitochondria. Our results indicate that hydrophobic bile acids induce apoptosis in HCT116 cells by releasing cytochrome c from mitochondria via an undefined but specific mechanism, and that UDCA protects HCT116 cells by acting downstream of cytochrome c release.