Effect of Torula Yeast (Candida utilis)-Derived Glucosylceramide on Skin Dryness and Other Skin Conditions in Winter.

Glucosylceramide (GlcCer) is present in foods such as barley, corn, and wheat flour. GlcCer derived from different foods has differences in its physiological effects, depending on the sphingoid backbone and constituent fatty acids. In this study, we investigated the moisturizing and skin conditioning effects of GlcCer derived from torula yeast (Candida utilis) in healthy human subjects. The participants were randomly distributed in a crossover, double-blind comparative manner. Seventeen volunteers were orally administered both 1.8 mg/d of GlcCer derived from torula yeast and a placebo for 4 wk. Before and after oral administration, transepidermal water loss (TEWL) was measured and the objective skin condition observation and a questionnaire on skin condition were conducted. The primary endpoint was TEWL; secondary endpoints included the objective and subjective skin conditions. The change in TEWL over the study period on the forearm was -0.97±0.48 and -1.26±0.46 g/m2•h in the placebo and GlcCer groups, respectively, with significantly lower (p=0.01) TEWL observed in the GlcCer group. Brown spots increased in the placebo group but significantly decreased in the GlcCer group (p=0.04). Although chapped skin worsened in the placebo group, it significantly improved in the GlcCer group (p=0.04). The use of torula yeast-derived GlcCer as a functional cosmeceutical food is a viable option to ameliorate skin conditions, including improvement in skin barrier function, reduction of brown spots, and fixation of chapped skin.

Increase in the protein-bound form of glutathione in human blood after the oral administration of glutathione.

The present study examined the impact of the supplementation of glutathione (GSH), γ-L-glutamyl-L-cysteinyl-glycine, on human blood GSH levels. Healthy human volunteers were orally supplemented with GSH (50 mg/kg body weight). Venous blood was collected from the cubital vein before and after ingestion. Plasma was mixed with 3 volumes of ethanol. The supernatant and precipitate were used for the deproteinized and protein fractions of plasma, respectively. Blood cell and plasma fractions were pretreated with 5% trichloroacetic acid-2% 2-mercaptoethanol to reduce the oxidized form of GSH and liberate protein-bound GSH. The 2-mercaptoethanol-pretreated GSH was determined by precolumn derivatization with 6-aminoquinolyl-N-hydroxy succinimidyl carbamate and liquid chromatography-tandem mass spectrometry. There was no significant difference in GSH contents in the deproteinized fraction of plasma and blood cell fraction after GSH ingestion. However, the GSH contents in the protein-bound fraction of plasma significantly (P<0.01) increased from 60 to 120 min after GSH supplementation.

Cancer preventive effects of vitamin E.

Vitamin E is well known as an antioxidant, with 8 natural isoforms, such as α-, bgr;-, γ- and δ-tocopherols and α-, ß-, gamma;- and δ-tocotrienols. It has been suggested that both tocopherols and tocotrienols have anti-tumor effects due to the antioxidant effect. The results of several studies have indicated that the tocotrienols may have a stronger bioactivity than the tocopherols. Both types have shown antiproliferative, proapoptotic and cyclooxygenase-2- inhibiting effects in in vitro studies. Several animal studies have demonstrated that vitamin E has cancer-preventing effects. However, clinical trials have not shown similar results for the cancer prevention effect of tocopherol. Although the Linxian Trials demonstrated that the supplementation of ß-carotene, α-tocopherol and selenium reduced cancer risk, the beneficial effects of α- tocopherol on prostate cancer disappeared after several years in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Vitamin E, especially tocotrienols, seems to be a potent agent for cancer prevention, however no large-scale clinical trial on the cancer prevention effect of tocotrienols has been conducted yet. Therefore it is expected that clinical trials overcoming the lower bioavailability of tocotrienols will be conducted, and it is urgently needed to assess the safety and the efficacy of the administration of the tocotrienols as a part of a cancer prevention regimen.

Chemoprevention of tocotrienols: the mechanism of antiproliferative effects.

Tocotrienols have been reported as antitumor agents and widely commercialized as an antioxidant dietary supplement. Tocotrienols have more significant biological activity than tocopherols, although serum level of tocotrienols is much lower than that of tocopherols. This may be because intracellular concentration of tocotrienols was revealed to be significantly higher compared with tocopherols, and tocotrienol accumulation is observed in tumor. Previous reports have suggested antiproliferative effect, induction of apoptosis, modulation of cell cycle, antioxidant activity, inhibition of angiogenesis, and suppression of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity as anticarcinogenesis mechanisms of tocotrienols both in vivo and in vitro. Extension of the duration of host survival was observed in tumor-implanted mice treated with tocotrienol. Tocotrienols induce apoptosis mainly via mitochondria-mediated pathway. Cell cycle arrest is due to suppression of cyclin D by tocotrienols. Tocotrienols also inhibit vascularization-reducing proliferation, migration and tube formation. Malignant proliferation demands elevation of HMG CoA reductase activity, and tocotrienols suppress its activity. Tocotrienol treatment decreases oncogene expression and increases the level of tumor suppressors. Only a few clinical trials to determine the effects of tocotrienol on cancer prevention or treatment have been carried out. There is no convincing or probable evidence of the role of tocotrienols in cancer prevention, while alpha-tocopherol has been suggested to have a limited anti-prostate cancer potential. Neither beneficial activity nor adverse effect of tocotrienol has sufficiently been explored so far. The above-mentioned mechanisms of tocotrienols seem to be promising for cancer prevention; however, further clinical studies are warranted to assess the efficacy and safety of tocotrienol.