Hepatic Alpha-tocopherol Research Articles

Antioxidant activity of dietary canthaxanthin

It has been suggested that canthaxanthin (CX), beta-carotene, and other carotenoids may inhibit carcinogenesis via antioxidant activity. CX has been shown to inhibit lipid peroxidation in liposomes; this experiment was designed to assess the antioxidant activity of CX in biological membranes. Chicks were fed semipurified diets supplemented with placebo beadlets or CX beadlets (5 g beadlets/kg diet; 0.5 g CX/kg diet) for five weeks. Diets were deficient in vitamin E and selenium to maximize the power of detecting an antioxidant effect of CX and to induce exudative diathesis, which is a vitamin E and selenium deficiency disease of chicks. Dietary CX had no effect on the onset, incidence, or severity of exudative diathesis. Liver homogenates from CX-fed chicks exhibited significantly (p = 0.02) decreased formation of thiobarbituric acid-reactive substances over time in ferrous ion-induced peroxidations. Because dietary CX increased hepatic alpha-tocopherol content, subsequent peroxidations were conducted in membrane fractions prepared from placebo and CX livers matched for alpha-tocopherol content. In this system, CX was marginally but inconsistently protective against peroxidation at both 15 torr O2 (p = 0.12) and 150 torr O2 (p = 0.07). Nanomolar changes in hepatic alpha-tocopherol, unlike CX, substantially altered rates of peroxidation. These results suggest that under these conditions, dietary CX increased resistance to lipid peroxidation primarily by enhancing membrane alpha-tocopherol levels and secondarily by providing weak direct antioxidant activity.

Influence of dietary vitamin E on the intermembrane transfer of alpha-tocopherol as mediated by an alpha-tocopherol binding protein.

The effect of dietary vitamin E on the intermembrane transfer of (3R)-alpha-tocopherol, a spontaneous process accelerated in the presence of an alpha-tocopherol binding protein (alpha TBP), was examined. The transfer activity of this cytosolic liver protein was assayed via in vitro transfer of (3R)-alpha-[3H]tocopherol (alpha[3H]T) from egg lecithin liposomes to human erythrocyte ghosts (EG). Male Fisher 344 rats (1 and 20 months old) were fed diets containing 0, 30, and 500 mg/kg vitamin E (dl-alpha-tocopheryl acetate) for 15 weeks. Liver cytosol fractions were assayed for alpha[3H]T transfer activity (alpha TTA). Among young rats, those fed vitamin E-deficient diets had the highest alpha TTA, 5.02 +/- 3.10 pmole alpha[3H]T/min (mean +/- SD), which was different (P less than 0.05) from the spontaneous transfer rate of 2.10 pmole/min. Neither young rats fed 30 and 500 mg/kg vitamin E diets nor any of the aged rats showed alpha TTA which differed significantly from the spontaneous transfer rate. To examine the relationship between hepatic alpha-tocopherol levels and alpha TTA, alpha-tocopherol concentration per gram of wet liver was assayed by HPLC. A steep positive slope (6.39 +/- 1.46 pmole min-1 nmole g-1) and strong correlation (r = 0.873) between hepatic alpha-tocopherol and alpha TTA were observed (P less than 0.005) among young vitamin E-deficient rats. The data indicates that alpha TTA varies directly with hepatic alpha-tocopherol concentration when total liver vitamin E stores are very low. Thus, alpha TBP-mediated transfer of alpha-tocopherol may be manifest only when vitamin E status is compromised.