Selenium is an essential micronutrient for humans, and seafood is one of the major selenium source in Japan. Recent studies show that the tissues of tuna and other predatory fish contain high levels of the selenium-containing imidazole compound, 2-selenyl-Nα, Nα, Nα-trimethyl-L-histidine (selenoneine). A substantial proportion of the total amount of selenium is present as selenoneine in the muscles of ocean fish. Selenoneine contains an imidazole ring with a unique selenoketone group and has an antioxidant activity in vitro and in vivo. The dietary intake of selenoneine through fish consumption is thought to be important for enhancing selenium redox functions in tissues and cells. In addition, selenoneine accelerated the excretion and demethylation of methylmercury through the formation of secretory extracellular lysosomal vesicles via the specific organic cation/carnitine transporter-1 (OCTN1). Dietary intake of selenoneine might decrease the formation of hydroxyl and other radicals and accelerate the excretion of heavy metals, and thereby inhibit carcinogenesis, lifestyle chronic diseases, and aging.
1.The plasma zinc disposition following administration of polaprezinc (Zinc L-Carnosine Complex) in six male subjects with an initial low serum zinc levels (<70 μg/dL) were compared to those in nineteen subjects with normal zinc levels. 2.The plasma zinc concentration reached a maximum plasma concentration (Cmax; 191 ± 30 μg/dL) at 1.83 h and returned to baseline level at 6 h after administration of 75 mg of polaprezinc (containing 17 mg of zinc). The plasma zinc concentration decreased at a half-life of 3.44 h. The area under the curve for plasma concentrations over time (0-12 h after administration; AUC0-12) was 1275 ± 138 μg•h-1•dL-1. 3.The plasma zinc level returned to the initial values at 6 h. It then decreased to values lower than those at baseline at 8 and 12 h following administration of polaprezinc. 4.In comparison with data from subjects with a normal zinc level, the absorption of zinc in subjects with low serum zinc following administration of polaprezinc was relatively low, and the deviation of AUC0-12 was minimal.
In patients with a renal failure, control of the absorption of dietary phosphate is necessary to prevent hyperphosphataemia. Recently, it has been proposed that ferric citrate is used as a phosphate-binder for patients with renal failure. However, several recent studies have indicated that an accumulation of iron in liver causes cirrhosis and liver cancer. In the present study, tissue iron deposition and serum transferrin saturation were examined in mature rats with long-term oral exposure to high dose of ferric citrate. Male 10-week old Wistar rats were fed AIN93M diet (basal diet) or the basal diet supplemented with 1.0% or 4.0% ferric citrate hydrate (FCH; iron content, 18.5%) for 24 weeks. Administration of FCH increased fecal phosphorus excretion dose-dependently. However, serum phosphorus concentrations in the FCH-exposed rats were not lower than those in the rats without exposure to FCH. Iron contents in the serum, liver, kidney and femur as well as transferrin saturation of rats fed the 4.0% FCH diet increased with the progress of feeding period and were significantly higher than those of the other rats. In particular, the hepatic iron deposition levels were increased to 3.3, 4.7 and 13.4 times higher than those in the rats without FCH exposure at the 4th, 12th and 24th week, respectively. Iron deposition levels in the spleen were dose-dependently increased by the FCH-exposure but saturated at the 12th week. Hemosiderin accumulation was observed in the liver cytoplasm of rats fed the 4.0% FCH rats and increased with progress of the exposure period. These results indicate that both of tissue iron deposition and increase of transferrin saturation occur when the iron exposure exceeds a threshold value; ferric citrate should be used as a phosphate-binder only in the case where the increase in transferrin saturation does not occur.
The purpose of this study was to investigate whether the zinc status of zinc-deficient rats is alleviated by restricted feeding of a zinc-deficient diet. A severe zinc-deficient diet (20% demineralized soy protein diet, ≦ 0.4 mg/kg Zn) was used in this experiment. Rats were fed either a zinc-deficient diet ad libitum (ZDA) or a 4.0 g/d zinc-deficient diet by restricted feeding (ZDR). ZDA rats stopped growing at day 4 after initiation of feeding. Body weight decreased and the cyclic feeding pattern ceased with food restriction. Survival time of rats fed a zinc-deficient diet was extended from 35 ±2.2 to 43 ±1.7 d (p<0.02). The results show that restricted feeding of a zinc-deficient diet alleviated zinc deficiency in rats. The body weight of zinc-deficient rats was decreased by food restriction, and zinc concentration increased in the serum, femur and carcass. In another experiment, zinc-deficient rats were fasted for 2 d. The body weight of zinc-deficient rats decreased rapidly, and the zinc concentration of serum, femur and carcass increased by fasting. Eventually, the decrease in body tissue resulted in an increase in zinc concentration and alleviated the zinc deficiency in rats.