An evaluation of surgically obtained skin (age range, 8-92 yr) revealed that there is an age-dependent decrease in the epidermal concentrations of provitamin D3 (7-dehydrocholesterol). To ascertain that aging indeed decreased the capacity of human skin to produce vitamin D3, some of the skin samples were exposed to ultraviolet radiation and the content of previtamin D3 was determined in the epidermis and dermis. The epidermis in the young and older subjects was the major site for the formation of previtamin D3, accounting for >80% of the total previtamin D3 that was produced in the skin. A comparison of the amount of previtamin D3 produced in the skin from the 8-and 18-yr-old subjects with the amount produced in the skin from the 77-and 82-yr-old subjects revealed that aging can decrease by greater than twofold the capacity of the skin to produce previtamin D3. Recognition of this difference may be extremely important for the elderly, who infrequently expose a small area of skin to sunlight and who depend on this exposure for their vitamin D nutritional needs.

We studied the incorporation and metabolism of eicosapentaenoic (EPA) and docosahexaenoic acid in six human volunteers who supplemented their normal Western diet for 5 mo daily with 10-40 ml of cod liver oil, rich in w-3 polyunsaturated fatty acids. EPA and docosahexaenoic acid were incorporated into the total phospholipids of plasma, platelets, and erythrocytes in a doseand time-dependent manner. During w-3 fatty acid ingestion serum triacylglycerols were lowered and platelet aggregation upon low doses of collagen was reduced. Concomitantly, formation and excretion of prostanoids showed a characteristic change. As measured in serum from whole clotted blood, thromboxane A3 was formed in small amounts, whereas thromboxane A2 formation was reduced to 50% of control values. Excretion of the main urinary thromboxane A metabolites was unaltered in subjects with low basal excretion rates, but decreased markedly in two subjects with high control values. As determined from the main urinary metabolite, prostaglandin I3 was formed from EPA at rates up to 50% of unaltered prostaglandin l2 formation. The biochemical and functional changes observed lasted for the entire supplementation period of 5 mo and were reversible within 12 wk after cessation of cod liver oil intake. Favorable changes induced by long-chain w-3 fatty acids include a dose-related and sustained shift of the prostaglandin I/thromboxane A balance to a more antiaggregatory and vasodilatory state.

This article is available online at http://www.jlr.org have used zebrafi sh to characterize the molecular consequences of vitamin E defi ciency because zebrafi sh require dietary ␣ -tocopherol, especially during embryonic development ( 2 ). Zebrafi sh also express the ␣ -tocopherol transfer protein ( ␣ -TTP), which facilitates hepatic ␣ -tocopherol secretion into the circulation in humans ( 3 ), and likely facilitates ␣ -tocopherol delivery from the yolk to the developing zebrafi sh embryo ( 4 ). Importantly, when the ␣ -TTP was knocked down in zebrafi sh embryos by 12-15 h postfertilization, the embryonic brain and eyes failed to form appropriately ( 4 ), indicating that ␣ -tocopherol is necessary for nervous system development. Further, during embryonic growth over 72 h both DHA (22:6) and arachidonic acid (AA) (20:4) decreased at faster rates in vitamin E-defi cient (E Ϫ ) compared with vitamin E-suffi cient (E+) zebrafi sh embryos ( 5 ). Moreover, adequate dietary ascorbic acid was necessary to prevent accelerated ␣ -tocopherol defi ciency and tissue damage ( 5 ).We hypothesized that the devastating effects of severe ␣ -tocopherol defi ciency in zebrafi sh embryos ( 4 ) are a result of depletion and alteration of critical brain lipids. Hypothetically, the brain, which is highly enriched in DHA yet cannot synthesize DHA to meet its needs ( 6 ), is highly susceptible to lipid peroxidation in the ␣ -tocopheroldefi cient state. It has been recognized for decades in humans that vitamin E defi ciency causes a progressive spinocerebellar ataxia ( 7 ). Moreover, Ulatowski et al. ( 8 ) have shown that vitamin E is necessary for preservation of Abstract We hypothesized that brains from vitamin E-defi cient (E ؊ ) zebrafi sh ( Danio rerio ) would undergo increased lipid peroxidation because they contain highly polyunsaturated fatty acids, thus susceptible lipids could be identifi ed. Brains from zebrafi sh fed for 9 months defi ned diets without (E ؊ ) or with (E+) added vitamin E (500 mg RRR -␣ -tocopheryl acetate per kilogram diet) were studied. Using an untargeted approach, 1-hexadecanoyl-2-docosahexaenoyl-sn -glycero-3-phosphocholine [DHA-PC 38:6, PC 16:0/22:6]was the lipid that showed the most signifi cant and greatest fold-differences between groups. DHA-PC concentrations were approximately 1/3 lower in E ؊ (4.3 ± 0.6 mg/g) compared with E+ brains (6.5 ± 0.9 mg/g, mean ± SEM, n = 10 per group, P = 0.04). Using lipidomics, 155 lipids in brain extracts were identifi ed. Only four phospholipids (PLs) were different ( P < 0.05) between groups; they were lower in E ؊ brains and contained DHA with DHA-PC 38:6 at the highest abundances. Moreover, hydroxy-DHA-PC 38:6 was increased in E ؊ brains ( P = 0.0341) supporting the hypothesis of DHA peroxidation. More striking was the depletion in E ؊ brains of nearly 60% of 19 different lysophospholipids (lysoPLs) (combined P = 0.0003), which are critical for membrane PL remodeling. Thus, E ؊ brains contained fewer DHA-PLs, more hydroxy-DHA-PCs, and fewer lysoPLs, suggesting t...

Dairy cows have increased nutritional requirements for antioxidants postpartum. Supranutritional organic Se supplementation may be beneficial because selenoproteins are involved in regulating oxidative stress and inflammation. Our objective was to determine whether feeding Se-yeast above requirements to Se-replete dairy cows during late gestation affects blood micronutrients, antioxidants, metabolites, and inflammation biomarkers postpartum. During the last 8-weeks before calving, dairy cows at a commercial farm were fed either 0 (control) or 105 mg Se-yeast once weekly (supranutritional Se-yeast), in addition to Na selenite at 0.3 mg Se/kg dry matter in their rations. Concentrations of whole-blood (WB) Se and serum Se, erythrocyte glutathione (GSH), and serum albumin, cholesterol, α-tocopherol, haptoglobin, serum amyloid A (SAA), calcium, magnesium, phosphorus, non-esterified fatty acids, and β-hydroxybutyrate were measured directly after calving, at 48 h, and 14 days of lactation in 10 cows of each group. Supranutritional Se-yeast supplementation affected indicators of antioxidant status and inflammation. Cows fed a supranutritional Se-yeast supplement during the last 8-weeks of gestation had higher Se concentrations in WB (overall 52 % higher) and serum (overall 36 % higher) at all-time points, had higher SAA concentrations at 48 h (98 % higher), had higher erythrocyte GSH (38 % higher) and serum albumin concentrations (6.6 % higher) at 14 days, and had lower serum cholesterol concentrations and higher α-tocopherol/cholesterol ratios at calving and at 48 h compared with control cows. In conclusion, feeding Se-replete cows during late gestation a supranutritional Se-yeast supplement improves antioxidant status and immune responses after calving without negatively impacting other micronutrients and energy status.