We have previously reported that substantial amounts of tocotrienols were present in the skin of animals fed a diet containing a tocopherols andtocotrienols rich fraction (T-mix) extracted from palm oil, and further, that sesame lignans enhanced tocotrienol levels in the skin. The present studies were undertaken to determine whether dietary tocotrienols and those with sesamin could protect the skin from damage induced by UVB irradiation in hairless mice fed four diets: a vitamin E-free diet, a 50 mg/kg alpha-tocopherol diet, a 229 mg/kg T-mix (with 50 mg alpha-tocopherol) diet and a 229 mg/kg T-mix with 2 g/kg sesamin diet. In Experiment 1, mice were fed the diets for 6 wk, and half of the mice were exposed to 180 mJ/cm(2 )of UVB light once daily for 7 d. After the intensity of sunburn was scored, vitamin E and thiobarbituric acid reactive substances (TBARS) concentrations in the skin and liver were determined. In Experiment 2, hairless mice were initiated with a single application of 7, 12-dimethylbenz[a]anthracene (DMBA), then 1 wk later mice were fed the experimental diets and subjected to 180 mJ/cm(2) UVB irradiation twice weekly for 20 wk. Tumor incidences were counted once a week. Tocotrienols were detected in the skin of mice fed T-mix, but their concentrations were significantly lower than for alpha-tocopherol. Sesamin elevated tocotrienol contents in the skin. In spite of the high alpha-tocopherol contents, the effects of alpha-tocopherol on sunburn and incidence of tumor were slight. T-mix fed groups reduced the extent of sunburn and incidence of tumor, and further reduction of sunburn and incidence of tumor were observed in the T-mix with sesamin group. These results suggest that dietarytocotrienols protect the skin more strongly than alpha-tocopherol against damage induced by UVB and sesamin enhances tocotrienol effects.
Familial dysautonomia (FD) is an inherited, fatal, neurodegenerative disorder manifested by autonomic/hypertensive crises and cardiac instability. Patients produce little IKAP, the gene product of the affected mutated gene, and have low levels of monoamine oxidase A (MAO A), whose reduced presence appears to result in an increased accumulation of biogenic amines, which is a trigger for hypertensive crises. As ingestion of tocotrienols elevates IKAP and MAO A in FD patients, we examined their impact on the frequency of hypertensive crises and cardiac function. After 3 to 4 months of tocotrienol ingestion, approximately 80% of patients reported a significant (> or = 50%) decrease in the number of crises. In a smaller group of patients, a postexercise increase in heart rate and a decrease in the QT interval were observed in the majority of participants. Based on these findings, we hypothesize that tocotrienol therapy will improve the long-term clinical outlook and survival of individuals with FD.