Biomedical subjects
Publications and source records attributed to N Hirose.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
9-(2-Azido-2,3-dideoxy-beta-D-threo-pentofuranosyl)adenine derivatives (1a-e) containing a lipophilic function at the N-6 position in the purine ring were prepared and evaluated for their antiviral activity. The compounds 1a-e turned out to be inactive as antiviral agents.
The effects of dietary supplementation of sesamin on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in female Sprague-Dawley rats were studied. Experimental diets containing 0.2% sesamin (an equiweight mixture of sesamin and episesamin) or 0.2% alpha-tocopheryl acetate were given to rats starting 1 week before intragastric administration of DMBA (10 mg/rat). Sesamin significantly (p less than 0.05) reduced the cumulative number of palpable mammary cancers by 36% at 12 weeks post-DMBA administration compared with animals on a control diet. Alpha-tocopheryl acetate inhibited both the incidence and the cumulative number of mammary tumors by 20% and 45%, respectively. Concentrations of lipid peroxides in plasma, liver and tumors were all decreased in both sesamin and alpha-tocopheryl acetate groups. The activity of peripheral blood mononuclear cells (PBMC) increased in rats fed sesamin (140 to 150% of the control and alpha-tocopheryl acetate groups). Fatty acid compositions of plasma, liver and tumor phosphatidylcholine showed a decreased tendency of the metabolism of linoleic acid to arachidonic acid and hence of the plasma concentration of prostaglandin E2 in the sesamin group. The inhibitory effect of sesamin on DMBA-induced mammary carcinogenesis may be ascribed, at least in part, to immunopotentiation and increased antioxidative activity.
The effect of dietary fats and cholesterol on dimethylbenz[a]-anthracene-induced mammary tumorigenesis was studied in female Sprague-Dawley rats. When the dietary fat source (at the 5% level) was palm oil (saturated fat) or corn oil (unsaturated fat), dietary cholesterol at the 0.2% level increased the tumor number of rats fed corn oil, but not those fed palm oil. Perilla oil (rich in alpha-linolenic acid) reduced tumor development as compared with safflower oil (rich in linoleic acid), but again dietary cholesterol at the 0.5% level diminished the favorable effect of n-3 polyunsaturated fatty acid (PUFA). The adverse effect of cholesterol was also observed in the n-6 PUFA fat. The promotive effect of dietary cholesterol was not necessarily associated with the change in the production of prostaglandin E2 by the tumor tissue or in the immunopotentiation. These results at least stress that the contrasting effects of dietary fats should be carefully evaluated whether cholesterol is present simultaneously or not.