The lack of HSD17B3 in male mice results in disturbed Leydig cell maturation and endocrine imbalance akin to humans with HSD17B3 deficiency.

Hydroxysteroid (17ß) dehydrogenase type 3 (HSD17B3) deficiency causes a disorder of sex development in humans, where affected males are born with female-appearing external genitalia, but are virilized during puberty. The hormonal disturbances observed in the Hsd17b3 knockout mice (HSD17B3KO), generated in the present study, mimic those found in patients with HSD17B3 mutations. Identical to affected humans, serum T in the adult HSD17B3KO mice was within the normal range, while a striking increase was detected in serum A-dione concentration. This resulted in a marked reduction of the serum T/A-dione ratio, a diagnostic hallmark for the patients with HSD17B3 deficiency. However, unlike humans, male HSD17B3KO mice were born with normally virilized phenotype, but presenting with delayed puberty. In contrast to the current belief, data from HSD17B3KO mice show that the circulating T largely originates from the testes, indicating a strong compensatory mechanism in the absence of HSD17B3. The lack of testicular malignancies in HSD17B3KO mice supports the view that testis tumors in human patients are due to associated cryptorchidism. The HSD17B3KO mice presented also with impaired Leydig cell maturation and signs of undermasculinization in adulthood. The identical hormonal disturbances between HSD17B3 deficient knockout mice and human patients make the current mouse model valuable for understanding the mechanism of the patient phenotypes, as well as endocrinopathies and compensatory steroidogenic mechanisms in HSD17B3 deficiency.

The Orbiting Carbon Observatory-2 early science investigations of regional carbon dioxide fluxes.

NASA's Orbiting Carbon Observatory-2 (OCO-2) mission was motivated by the need to diagnose how the increasing concentration of atmospheric carbon dioxide (CO2) is altering the productivity of the biosphere and the uptake of CO2 by the oceans. Launched on 2 July 2014, OCO-2 provides retrievals of the column-averaged CO2 dry-air mole fraction ([Formula: see text]) as well as the fluorescence from chlorophyll in terrestrial plants. The seasonal pattern of uptake by the terrestrial biosphere is recorded in fluorescence and the drawdown of [Formula: see text] during summer. Launched just before one of the most intense El Niños of the past century, OCO-2 measurements of [Formula: see text] and fluorescence record the impact of the large change in ocean temperature and rainfall on uptake and release of CO2 by the oceans and biosphere.

Effect of selenium fertilization on selenium in feedstuffs and selenium, vitamin E, and beta-carotene concentrations in blood of cattle.

Selenium (n = 56), total vitamin E, and homologues of natural vitamin E in feedstuffs (n = 52) and the concentrations of Se (n = 241), vitamin E (n = 244), and beta-carotene (n = 227) in blood were measured. The mean (+/- SD) Se content in hay, grass silage, oats, and barley produced using fertilizers enriched with Se was 0.13 (+/- 0.169), 0.17 (+/- 0.704), 0.23 (+/- 0.107) and 0.21 (+/- 0.119) mg/kg of DM, respectively, and the mean (+/- SD) vitamin E contents, calculated as dl-alpha-tocopherol acetate equivalents, were 39.7 (+/- 13.0), 120.0 (+/- 40.27), 24.4 (+/- 3.83) and 34.5 (+/- 3.57) IU/kg of DM, respectively. The mean Se concentrations in whole blood of cows, heifers, bulls and calves fed hay (n = 62), silage (n = 111), or pasture (n = 68) varied from 183 to 244 micrograms/l. The mean concentrations of total vitamin E in serum of lactating cows fed hay (n = 21), silage (n = 29) or pasture (n = 26) were 2.8 (+/- 1.43), 6.5 (+/- 3.03) and 8.2 (+/- 2.64) mg/l, respectively. For calves, concentrations of vitamin E in serum were as low as 0.25 mg/L. The mean concentration of beta-carotene in serum of lactating cows fed grass silage (n = 26) or pasture (n = 28) was 13.7 (+/- 6.61) and 15.4 (+/- 6.15) mg/L, respectively, but, in lactating cows fed hay (n = 20), concentrations were 2.5 (+/- 1.07) mg/L.

Blood selenium, vitamin E, vitamin A, and beta-carotene concentrations and udder health, fertility treatments, and fertility.

We investigated the activity of glutathione peroxidase in whole blood; concentrations of vitamin E, vitamin A, and beta-carotene in serum; SCC; udder bacterial infections and the incidence of clinical mastitis; fertility treatments; and the success of first AI of 511 dairy cows for 1 yr. The mean Se content in whole blood and the concentrations of vitamin E, vitamin A, and beta-carotene concentrations in serum were 191 micrograms/L, 5.9 mg/L, 0.39 mg/L, and 12.9 mg/L, respectively. An increase in Se concentration in whole blood was associated with a decrease in all infections, including infections by Staphylococcus aureus, Actinomyces pyogenes, and Corynebacterium spp. (-17.7, -31.7, and -70.6%, respectively). There was no association among the different infections or SCC and concentrations of vitamin E, vitamin A, or beta-carotene, but an association existed between vitamin A concentration and SCC. The lower Se concentration in whole blood did not increase incidence of clinical mastitis. The Se concentration in whole blood (200 micrograms/L) was accepted as a target value to optimize udder health. The incidence of fertility disorders (anestrus, subestrus, cystic ovaries, or delayed ovulation) was 34.4%. The pregnancy rate following first insemination was 48.6%. No significant association was observed among Se in whole blood; concentrations of total vitamin E, vitamin A, or beta-carotene in serum; and fertility disorders or success of first AI.

Biopotency of vitamin E in lucerne meal for chickens.

In order to estimate the biopotency of vitamin E in lucerne/alfalfa meal in comparison to that of dl-alpha-tocopheryl acetate (dl-alpha-Ta; all-rac-alpha-Ta) a study was conducted with newly hatched White Leghorn male chicks. An increase in the vitamin E level in the liver and plasma, and the prevention of nutritional encephalomalacia (NE) were used as criteria for biopotency. After a vitamin E depletion period of one week posthatching, the chicks continued on a semipurified, vitamin E free basal diet without vitamin E supplementation, or were repleted with graded levels of that vitamin for six weeks, provided as extracted lucerne oil or as dl-alpha-Ta. High performance liquid chromatography (HPLC) with fluorescence detection was used for the analysis of the vitamin E homologues. The diagnosis of NE was based on clinical and histopathological observations. A significant increase (P < 0.05) in vitamin E content in the liver and plasma was observed in response to dietary supplementation with both vitamin E sources. The linear increase both in the liver and plasma storage assays was associated with a reduced incidence of NE. The disease was totally prevented by a dietary supplement of 7.50 and 5.40 mg vitamin E/Kg feed provided as dl-alpha-Ta or lucerne oil, respectively. The natural biopotency of the vitamin E in lucerne meal compared with that of dl-alpha-Ta in the liver and plasma storage assays and in the prevention of NE was 123, 105 and 99%, respectively, as calculated by the slope ratio technique.

Effect of vitamin E supplementation on weight gain, immune competence, and disease incidence in barley-fed beef cattle.

The aim of the study was to investigate whether vitamin E supplements in larger amounts than recommended could reduce incidence of disease, improve immune competence, and increase rate of weight gain of conventionally barley-fed beef cattle. Mean daily intake of vitamin E by individual calves in the experimental group was 200 mg during the first 2 mo, 400 mg during the next 2 mo, and 600 mg during the rest of the period. Corresponding daily intakes of vitamin E for the control group were 50, 100, and 150 mg. Mean plasma vitamin E of the experimental group increased from .49 mg/L at the start of the trial to 2.03 mg/L at the end, but that of the control group was lower at the end (.36 mg/L) than at the beginning (.53 mg/L). No significant differences were observed between the groups concerning incidence of disease or magnitude of lymphocyte stimulation. The results indicated that there was a surprisingly poor biological availability of the dietary vitamin. Therefore, a comparison in reality was made between calves with inadequate and normal vitamin E status. The differences in daily BW gain and time to reach slaughter weight thus probably were effects of the low vitamin E status rather than positive effects of additional vitamin in the diet.

Histopathological and biochemical changes associated with selenium and vitamin E deficiency in chicks.

One day old unsexed White Leghorn chicks obtained either from commercial hens fed adequate levels of selenium (Se) and vitamin E (VE) (Comm. chicks), or from hens depleted in both nutrients (Depl. chicks), were fed a low Se-VE semi-synthetic basal diet. The dietary Se content was kept constantly low, while graded levels of VE as dl-alpha-tocopheryl acetate (dl-alpha Ta), (0, 5, 10 or 15 mg VE/kg diet) were fed for six weeks. An efficient carry-over of Se and VE from hens to their progeny was observed by a significant increase in their muscle Se, liver Se-glutathione peroxidase (Se-GSH-Px), and VE content at hatching. In the Depl. chicks, signs of Se-VE deficiency, i.e. exudative diathesis (ED) were observed at hatching, indicating that the deficiency lesions had developed during the embryonic period, whereas these signs were not observed in Comm. chicks on the depletion diets until they were 2 weeks old. The VE supplemental level of 15 mg/kg was not adequate to provide a complete protection against ED. Exudative diathesis was associated with low levels of muscle Se, liver Se-GSH-Px and VE and was also accompanied by a simultaneous increase in the liver non-Se-GSH-Px. Autopsy findings and histopathological lesions were observed only in subcutaneous tissue and skeletal muscle. The subcutaneous tissue was edematous with hyaline vascular lesions and hemorrhages. The thigh muscles were more susceptible to deficiency lesions than were the breast muscles, and showed in acute stages degenerative processes of the muscle fibers including calcium deposits, vascular lesions and hemorrhages. In subacute and chronic cases, reparative changes and muscle damage may develop independently of the hyaline vasculosis. To prevent ED, adequate Se and VE in chick diet is essential after hatching, irrespective of their tissue reserves of both nutrients at 1 day of age.

The vitamin E distribution in serum, liver, adipose and muscle tissues in the pig during depletion and repletion.

This study was designed to examine the storage capacity for vitamin E in liver, adipose tissue and skeletal muscle of growing pigs during a period of supplementation and of depletion. Therefore, biopsy specimens of these tissues and samples of serum were frequently taken from 7 pigs throughout the experimental period. After a 7-week period on a diet highly supplemented with vitamin E (405 mg/kg), a significant increase (p less than 0.001) in the concentration of this vitamin was observed in all tissues sampled. The highest level (102.9 +/- 26.2 mg/kg) was observed in the liver. After 2 days of depletion the concentration of vitamin E in the liver had fallen by 80%, whereas the concentration in the fat and muscle remained unchanged during 1 week of depletion. The serum vitamin E value rose significantly (p less than 0.001) after 1 week on the supplemented diet and then remained at about 7 mg/l throughout the supplementation period and decreased (p less than 0.001) after 2 days on a nonsupplemented diet. Generally, the serum vitamin E levels among growing pigs are between 2 and 3 mg/l. The results show that the serum and liver values were correlated when the serum level was within this range. Moreover, it is clearly demonstrated that the concentrations of vitamin E in serum and liver reflect the immediate nutritional status of the animal, whereas the vitamin concentrations in adipose and skeletal muscle tissue reflect its long-term nutritional history.

Vitamin E status in newborn lambs with special reference to the effect of dl-alpha-tocopheryl acetate supplementation in late gestation.

Pregnant ewes were supplemented with dl-alpha-tocopheryl acetate, either as a single intramuscular dose (500 mg two weeks before lambing) or perorally (150 mg daily during 3-4 weeks before lambing). Ewes without such a supplementation were controls. The vitamin E supplemented ewes had nearly twice as high vitamin E (alpha-tocopherol) concentrations as the unsupplemented control ewes at lambing both in serum and in colostrum. The vitamin E concentration in colostrum was 5-11 higher than in milk 1 week after lambing. Both supplementations somewhat increased the vitamin E serum concentration of the newborn lambs, but the increase was negligible in comparison with the effect produced by the consumption of colostrum. All lambs had very low serum concentrations at birth. The lambs from the supplemented ewes had significantly higher serum values than the control lambs 24 h after birth. The ewes had somewhat higher selenium status at birth than their offsprings when evaluated by glutathione peroxidase (GSH-Px) in the erythrocytes. It seems reasonable that nutritional muscular degeneration may arise in newborn lambs with a normal selenium status if their vitamin E status is critical, either because of an inadequate consumption of colostrum or because of a vitamin E deficient diet during pregnancy with a low vitamin concentration of colostrum as a consequence.

Response of whole blood, erythrocyte and plasma vitamin E content to dietary vitamin E intake in the chick.

Whole blood, red blood cells (RBC), and plasma vitamin E (VE) levels in chicks fed dietary VE (dl-alpha-tocopheryl acetate, dl-alpha Ta) supplementation in steps of 0.0, 5.0, 10.0, 15.0, 20.0 and 30.0 mg/Kg were determined to examine their usefulness as an index of VE status. The increase in VE level was significant and linear in whole blood (r = 0.90), RBC (r = 0.89) and plasma (r = 0.93) in response to dietary VE intake. There was a close correlation between VE in plasma vs whole blood (r = 0.90), plasma vs RBC (r = 0.91) and whole blood vs RBC (r = 0.95). The plasma VE content was 1.2-1.8 times greater than that of whole blood, and 6.6-12.5 times greater than that of RBC. The plasma total lipids content was not affected by the dietary VE intake, whereas the level of VE in the plasma total lipids was significantly increased with increasing supplementation. Alpha tocopherol was the major isomer (ca 92%) of VE in whole blood, RBC and plasma at hatching. The small proportions of beta-tocopherol (ca 2%), gamma-tocopherol (ca 5%) and alpha-tocotrienol (ca 1%) observed at 1 day of age had decreased or totally disappeared by 7 days of age after feeding the VE-free basal diet. The data showed that in the chick, the whole blood and RBC levels of VE were as sensitive and reliable indexes of dietary VE status as was that of the plasma.

Vitamin E requirement of growing swine.

The vitamin E requirement of growing pigs was estimated on the basis of prevention of morphological signs of deficiency. Five groups of pigs were fed a barley-based diet low in vitamin E that contained 16 mg of DL-alpha-tocopheryl acetate equivalents/kg and .1 ppm of Se for 4 wk (depletion I). This period was followed by 7 wk of supplementation, during which the groups received 0, 15, 45, 135 and 405 mg of supplemental DL-alpha-tocopheryl acetate/kg diet. Finally, all the animals were fed the low vitamin E diet for 7 wk (depletion II). To follow the vitamin E concentration in serum and tissues, blood samples were collected and biopsies were taken from skeletal muscle, adipose tissue and the liver throughout the experiment. The peak vitamin E value was observed in the liver, followed by the adipose tissue and then skeletal muscle. The liver responded rapidly to changes in dietary vitamin E intake, whereas the adipose tissue and the skeletal muscle reacted at a slower rate. In spite of the abundant occurrence of the different vitamin E isomers in the feed, alpha-tocopherol was the main isomer detected both in the serum and in the tissues. The activity of glutathione peroxidase in serum increased with age but was independent of the serum vitamin E concentration. In the unsupplemented group all animals suffered from the vitamin E and Se deficiency syndrome (VESD) in an acute or chronic form. A total of 31 mg of DL-alpha-tocopheryl acetate/kg diet (16 mg of naturally occurring vitamin E and 15 mg as supplementation) equivalent to 2.5 IU vitamin E/g polyunsaturated fatty acids (PUFA) was enough to prevent the development of VESD. In view of the large individual variations of vitamin E concentration in target organs, and to obtain a certain safety margin for prevention of VESD in growing pigs, a supplement of 30 mg of DL-alpha-tocopheryl acetate/kg diet is recommended.

Nutritional muscular degeneration in young heifers.

Young heifers with nutritional muscular degeneration had relatively low serum tocopherol values despite being on pasture which contained high levels of vitamin E. One possible explanation may be that vitamin E was destroyed within the rumen, another that the clinical symptoms arose very soon after turning out the animals.

Vitamin E requirement of mink with special reference to tocopherol composition in plasma, liver, and adipose tissue.

Tissue responses of 4 different tocopherols found in a basal diet (BD) and the effect of 2 physiologic levels of dl-alpha-tocopheryl acetate (25 and 150 mg/kg) on tissue tocopherol content were studied in the mink. The BD contained a total of 7.1 mg vitamin E/kg, with alpha-, beta-, gamma-, and delta-tocopherol in a ratio of 1:0.07:0.55:0.10, respectively. The corresponding ratios in the tissues were: liver, 1:0.04:0.12:0; plasma, 1:0:0.13:0; and adipose tissue, 1:0:0.19:0. After mink were fed diets containing vitamin E, alpha- and gamma-tocopherol were distributed in similar proportions in plasma and liver, but gamma-tocopherol was in a slightly higher proportion in adipose tissue. Addition of 25 or 150 mg/kg of alpha-tocopheryl acetate to the BD decreased the gamma-tocopherol levels in all 3 tissues; this was considered to be a dilution effect of other tocopherols in BD with added alpha-tocopheryl acetate. The beta-tocopherol content in the liver remained unchanged, irrespective of the dietary amount of alpha-tocopheryl acetate. Plasma alpha-tocopherol had a linear relationship to log dietary dose, with an apparent half-saturation of the vitamin E binding capacity at 13 mg vitamin E/kg diet. At the given dietary levels, liver and adipose continued to accumulate alpha-tocopherol. The correlation between total plasma lipids and plasma alpha-tocopherol was significant (P less than 0.001) only in the group fed the BD. Vitamin E analysis of plasma could be used as a routine method for controlling the vitamin E status of mink.(ABSTRACT TRUNCATED AT 250 WORDS)