Katsuhiko Noda

Ginkgo biloba extract protects brain neurons against oxidative stress induced by hydrogen peroxide.

Effect of Ginkgo biloba extract was examined on dissociated rat cerebellar neurons suffering from oxidative stress induced by hydrogen peroxide using a flow cytometer and ethidium bromide. Hydrogen peroxide at a concentration of 3 mM increased the number of neurons stained with ethidium (presumably dead neurons) in a time-dependent manner. Pretreatment of neurons with G. biloba extract (10 micrograms/ml) greatly delayed a time-dependent increase in number of dead neurons during exposure to hydrogen peroxide. It was true, but less effective, in the case of treatment with G. biloba extract immediately or 60 min after start of oxidative stress. Results implicate G. biloba extract as a potential agent in protecting the neurons suffering from oxidative stress induced by hydrogen peroxide.

Selenium intake based on representative diets in Japan, 1957 to 1989

Abstract Daily selenium (Se) intake during the past few decades in Japan was studied to obtain information toward establishing the daily selenium requirement. Three daily model menus of each year were prepared based on the daily per capita consumption of foods and nutrient intake from national surveys conducted in Japan in 1957, 1966, 1977, 1983 and 1989. The average daily intakes of Se found were 98 ± 33, 138 ± 7, 163 ± 31, 120 ± 18 and 129 ± 23 μg per capita, respectively. During this period, the decrease in Se intake from cereals was compensated by an increase in the intake from animal products: meats, eggs and dairy products. Thus, the amount of daily Se intake did not change markedly, averaging 129 ± 32 μg per capita during 1957 to 1989.

The effect of protein depletion on the rate of protein synthesis in rat liver

In order to understand the mechanism of decreased protein synthesis in the liver of rats fed a protein-free diet, the average polypeptide chain assembly time (tc) was measured by the method of Mathews et al. (J. Biol. Chem. (1973) 248, 1329). For rats fed a normal diet, tc in liver in vivo was 1.28 min. A 10-day period of protein depletion led to a value of tc = 2.08 min, corresponding to a 38% depression in polypeptide elongation rate. Protein depletion caused an extensive breakdown of hepatic polysomes and refeeding of a complete mixture of amino acids resulted in rapid recovery of polysomal profile. But tc in the liver of the refed animals gave still depressed value of 1.95 min. The amount and size distribution of poly(A)-containing mRNA in the liver, as determined by [3H]poly(U) hybridization, were the same for normal and depleted groups. These results suggest that both initiation and elongation steps of protein synthesis are depressed in the liver of protein-depleted rats. Refeeding of amino acid mixture rapidly restores initiation but not elongation activity.