雄激素受体在雄性激素源性脱发患者的表达观察

目的：了解雄激素受体（AR）在雄性激素源性脱发（AGA）患者顶部表皮、毛囊、皮脂腺、汗腺中的表达情况。方法：选取26例雄性激素源性脱发患者顶部、枕部以及10例非脱发者的顶部头皮标本,用免疫组织化学检测表皮、毛囊、皮脂腺、汗腺中AR的表达。结果：脱发患者头顶部毛囊、皮脂腺、汗腺AR表达均明显强于枕部和非脱发者枕部,差异均有统计学意义（P〈0.05）;脱发患者枕部毛囊、皮脂腺、汗腺AR表达与非脱发者顶部AR表达比较差异均无统计学意义（P〉0.05）;所有标本表皮中AR均为阴性。结论：AR在AGA患者头顶部毛囊、皮脂腺、汗腺的高表达,可能是AGA重要原因之一。     

Vitamin A in Skin and Hair: An Update

Vitamin A is a fat-soluble micronutrient necessary for the growth of healthy skin and hair. However, both too little and too much vitamin A has deleterious effects. Retinoic acid and retinal are the main active metabolites of vitamin A. Retinoic acid dose-dependently regulates hair follicle stem cells, influencing the functioning of the hair cycle, wound healing, and melanocyte stem cells. Retinoic acid also influences melanocyte differentiation and proliferation in a dose-dependent and temporal manner. Levels of retinoids decline when exposed to ultraviolet irradiation in the skin. Retinal is necessary for the phototransduction cascade that initiates melanogenesis but the source of that retinal is currently unknown. This review discusses new research on retinoids and their effects on the skin and hair.     

Adolescent vitamin A intake alters susceptibility to mammary carcinogenesis in the Sprague-Dawley rat

We tested the hypothesis that adolescent dietary vitamin A intake impacts mammary gland development and subsequent sensitivity to carcinogenesis. Sprague-Dawley rats were fed a purified diet that was vitamin A deficient, adequate (2.2 mg retinyl palmitate/kg diet), or supranutritional (16 mg retinyl palmitate/kg diet) from 21 to 63 days of age, the period of adolescent mammary gland development. At 73 days of age, rats were given 1-methyl-1-nitrosourea (25 mg/kg body wt i.p.) and monitored for mammary tumors. Tumors appeared earlier and more frequently in rats fed vitamin A-deficient or -supplemented diets. Vitamin A deficiency during adolescence was associated with alveolar mammary gland development and precocious milk protein expression, while supplementation was associated with ductal gland development and suppression of milk protein expression. Differences in circulating estradiol and mammary gland estrogen receptor-alpha, and estrogen-responsive progesterone receptor mRNA were not observed, suggesting that the effects of vitamin A on mammary gland development and carcinogenesis are estrogen independent. Mammary expression of another hormone receptor that regulates milk protein expression, the glucocorticoid receptor, was also unaffected. These results demonstrate that vitamin A intake during adolescence alters mammary gland differentiation and indicate that a narrow range of vitamin A intake during adolescence protects against carcinogenesis.     

Novel interactions of vitamin E and estrogen in breast cancer

The prevention of breast cancer through dietary modification is an active area of clinical and epidemiological research. It has been proposed that dietary supplementation of vitamin E may reduce a woman's risk of developing breast cancer. However, the exact mechanism remains unknown. alpha-Tocopherol is the most biologically active form of vitamin E. We investigated the effect of vitamin E (alpha-tocopherol) on breast cancer cell growth. A dose-dependent inhibition of cell proliferation was found in estrogen receptor (ER)-positive cells showing a potent suppression of growth at 100 microM vitamin E in MCF-7 (53%) and T47D (75%) cells. Vitamin E reduced significantly the response of both cell lines to estrogen (10 nM), and cell proliferation was decreased in MCF-7 and T47D cells by 69% and 84%, respectively. No growth inhibition was observed when cells were grown in the absence of estrogen. Vitamin E altered and decreased the growth inhibition induced by tamoxifen (10 microM) in MCF-7 (33%) and T47D (54%) cells. In addition, the immunostaining of ER of MCF-7 cells was reduced by 30% in the presence of vitamin E, suggesting an effect of vitamin E on the expression of ER. This provides evidence that vitamin E may inhibit ER-positive cell growth by altering the cellular response to estrogen.     

Altered lipoprotein metabolism in spontaneous vitamin E deficiency of owl monkeys

Certain owl monkeys (AOT) develop spontaneous hemolytic anemia that responds to vitamin E. The anemia is associated with red blood cell lipid peroxidation and altered red blood cell membrane lipid composition. To investigate these changes, plasma lipid and lipoprotein profiles were characterized in anemic, anemia-susceptible, and anemia-resistant AOT. The plasma vitamin E and vitamin A concentrations were assessed as an index of fat absorption and the effect of corn oil supplementation and vitamin E-selenium injection were measured. Anemia-susceptible AOT had depressed plasma levels of vitamin E and A and an altered lipoprotein metabolism characterized by elevated ratios of low/high density lipoprotein cholesterol and free to esterified cholesterol in these lipoproteins. Vitamin E-selenium injection in anemia-susceptible AOT increased the plasma vitamin E, and vitamin E and corn oil supplements reduced the high density lipoprotein free to esterified cholesterol ratio. The data suggest that the AOT suffer from fat malabsorption and that the consequences (including tocopherol deficiency) result in altered cholesterol metabolism.     

Vitamin D Interactions with Soy Isoflavones on Bone after Menopause: A Review

Vitamin D is known to increase Ca absorption in adults. However, the threshold vitamin D status to benefit Ca absorption is lower than the target vitamin D status for higher bone mineral density and lower fracture risk, pointing to another pathway for vitamin D to benefit bone. One possibility is by affecting osteoblast and osteoclasts directly. Vitamin D-related bone metabolism may also be affected by soy isoflavones, which selectively bind to the estrogen receptor β and may reduce bone loss in postmenopausal women. We discuss a possible synergistic effect of soy isoflavones and vitamin D on bone by affecting osteoblast and osteoclast formation and activity in postmenopausal women.     

硒、维生素A、E对人类乳腺癌细胞增殖的影响

本文研究了Se、VA和VE及其联合作用对人类乳腺癌细胞BCaP-37增殖的影响,结果提示Se对该细胞的增殖有双向作用,浓度高于5μM抑制细胞生长,低于该浓度则刺激细胞生长。醋酸维生素A酯浓度在1.0—10.0mg/L范围内对该细胞生长有明显的抑制。维生素A酸对该细胞的生长仅有很弱的抑制作用。VE对细胞也有弱抑制生长的作用。在稍高于生理浓度的水平下,Se(5μm)与VA(2mg/L)和VE(20mg/L)三者联合处理细胞,细胞核酸含量明显降低,提示Se、VA和VE能协同抑制BCaP-37细胞的增殖,而且这种抑制有可逆的趋势。联合使用Se和VA或VE未观察到二者间对细胞生长有协同抑制。上述结果表明联合使用Se、VA和VE对乳腺癌的防治可能是有益的。     

INTERRELATIONSHIPS BETWEEN VITAMINS A AND E

Large doses of vitamin A deplete hepatic and serum alpha-tocopherol in rats. Vitamin A deficiency in chicks alters protein metabolism and yet enhances incorporation of amino acids into protein, unless large amounts of vitamin E are fed. These effects may result from altered membrane permeability.     

Why do we have apocrine and sebaceous glands?

The secretions of sebaceous and apocrine glands fulfil an important thermoregulatory role in cold-stressed and heat-stressed hunter-gatherers. In hot conditions the secretions emulsify eccrine sweat and thus encourage the formation of a sweat sheet and discourage the formation and loss of sweat drops from the skin. In colder conditions sebum changes its nature and repels rain from skin and hair.     

Vitamin A in the urine of carnivores

Vitamin A levels (retinol equivalents) in the urine of canines were between 423 ng/ml (dog) and 6304 ng/ml (silver fox). Neither vitamin A nor vitamin E was found in the urine of herbivores, omnivorous and rodents. No vitamin A but low levels of vitamin E were detected in cats. Vitamin A in the urine was present as retinol and retinyl esters (basically retinyl palmitate/oleate). The total excretion of vitamin A represented 15 to 63% of the daily uptake in dogs, while less than 4% of vitamin E was excreted. Results after precipitation and ultracentrifugation indicate that similar carrier proteins may exist for retinol, retinyl esters and alpha-tocopherol in the urine. The biological significance of this phenomenon is discussed with regard to the high concentrations of retinyl esters in the blood plasma of carnivores bound to lipoproteins.     

Effect of an oral dose of vitamin E on the vitamin E and cholesterol content of tissues of the vitamin E-deficient rat

Weanling rats (female Sprague-Dawley) were fed until maturity a vitamin E-deficient diet or the deficient diet supplemented with 66 IU RRR-alpha-tocopheryl acetate/kg. Vitamin E, vitamin E quinone and total cholesterol levels in plasma, liver, paraovarian adipose tissue, lung, ovary and adrenal tissue were measured by high performance liquid chromatography. Vitamin E levels were greatly diminished, but cholesterol levels were unchanged in all tissues except adipose tissue of animals fed the deficient diet. Vitamin E-deficient animals received a single oral dose of 2 or 16.7 mg of RRR-alpha-tocopherol, and tissues were examined at 12 and 48 h. Plasma and liver formed a vitamin E pool that peaked at 12 h, had a high vitamin E/cholesterol ratio at 12 h and contained only trace amounts of vitamin E quinone. Adipose tissue, lung, ovary and adrenal concentrated vitamin E throughout the 48-h period, had low vitamin E/cholesterol ratios and contained small but significant amounts of vitamin E quinone. Vitamin E levels (micrograms/gram) at 48 h in lung, ovary and adrenal were higher than the vitamin E level in liver but the liver contained much more vitamin E (micrograms/organ) than the other tissues combined. Cholesterol levels (micrograms/gram) in plasma and liver decreased 45 to 55% in a dose- and time-dependent manner when a single oral dose of vitamin E was administered to deficient animals. Cholesterol levels in adipose tissue, lung and ovary were unchanged while the cholesterol level in adrenal increased 122% in a time-dependent manner with a single oral dose of vitamin E. These data show that a single oral dose of vitamin E has a profound effect on cholesterol levels in short-time experiments with the vitamin E-deficient rat. This rat model is appropriate for studies on the relationship between vitamin E and cholesterol metabolism in plasma, liver and the adrenal.     

Vitamin C status and nutrient interactions in a healthy elderly population

Vitamin C status and interactions with other nutrients were studied in 677 healthy, noninstitutionalized elderly people aged 60-98 y. Although 6% of the males and 3% of the females showed marginal vitamin C status (plasma ascorbic acid 11 to less than 23 mumol/L), only one person had a plasma ascorbic acid (AA) level less than 11 mumol/L. At all levels of total vitamin C intake, mean plasma AA levels were higher in females than males. Vitamin C supplement use was associated with generally higher blood levels of vitamins B-6, B-12, and E and folate in both sexes and with higher levels of retinol in females. However, after both age and the total dietary intake of the specific nutrient being examined were controlled for, plasma AA levels were significantly correlated only with plasma levels of vitamin E and folate in females.     

Possible vitamin B6 deficiency in nigerian young adults: Assessment by xanthurenic acid excretion

Vitamin B₆ status was assessed from urinary xanthurenic acid (XA) excretion in 34 male and female university students in Nigeria. Urinary XA excretion was measured following a 5g L-tryptophan load administered before (pre-pyridoxine) supplementation. About 95% of the females and 35% of the males excreted above 150 umoles XA/24hr (indicative of vitamin B₆ deficiency) after tryptophan loading. Supplementation with 25mg pyridoxine hydrochloride for 2 days significantly reduced XA excretion in all subjects; the reduction was more significant for females than males. In view of the wide-spread deficiency of riboflavin in Nigeria, and the involve-of riboflavin in pyridoxine metabolism, it is speculated that riboflavin status in addition to hormonal influence (in females) may account for the high occurrence of vitamin B₆ deficiency in these subjects.     

Different responses of the submandibular salivary glands and liver of rats subjected to excess vitamin A: study on glycogen metabolism

The effect of excess vitamin A on glycogen metabolism in the submandibular salivary gland, as compared to that in liver was studied. Contrary to what has been previously reported for the liver, either using from 1 to 6 X 15 000 or 2 X 30 000 U.I. vitamin A, the glycogen content in the submandibular salivary gland was lower in the hypervitaminotic rats. The total phosphorylase activity was reduced in the groups receiving lower vitamin A doses.     

手术创伤病人维生素A、E的补充

观察了食道癌、胃癌、肺癌、脓胸等18例病人术后补充维生素的结果.按维生素A(VA)15000IU/d;维生素E(VE)100mg/d剂量补充1～3周,测定血清中VA、VE及脂质过氧化物(LPO)的含量.结果提示;胸腹部手术创伤病人,补充上述剂量维生素后,可使血清VA、VE浓度维持在良好的营养水平.但尚不能使血清LPO下降至正常水平.同时对病人手术前的膳食提出了建议.     

维生素D缺乏与女性生殖关系的研究进展

维生素D在体内不止作为维生素，也可以作为激素发挥作用。它是一种可以调节钙磷代谢的固醇类衍生物，在心血管疾病、免疫调节、抗炎、癌症、生殖等各方面都能发挥一定的生物学作用。该生物学作用通常通过可溶性蛋白维生素D受体（VDR）来实现。VDR是一种位于靶细胞核内的转录因子，分布在人类各种系统组织中，包括女性生殖系统。近年有关维生素D与女性生殖系统的关系引起人们关注。维生素D一定程度上影响卵巢生理功能及女性生育力，同时与一些女性生殖系统疾病有关，如多囊卵巢综合征、子痫前期、子宫内膜异位症、妊娠期糖尿病等。现就维生素D缺乏与女性生殖系统关系的相关研究进行综述。     

Vitamin E: absorption, plasma transport and cell uptake

PURPOSE OF REVIEW: Large-scale clinical trials have failed to demonstrate a benefit for vitamin E supplementation in cardiovascular prevention. This contrasts with previous epidemiological studies indicating that individuals with high vitamin E status benefit from protection against chronic illnesses, including cardiovascular diseases. These conflicting results suggest that the metabolism of supplemental versus naturally delivered vitamin E and their potential roles, other than a potent antioxidant action, are not fully understood. The purpose of this review is to provide an update on current knowledge on the intestinal absorption of vitamin E, its plasma transport and its supply to cells. The review will also discuss the intravascular metabolism of intravenously delivered vitamin E. RECENT FINDINGS: Although the luminal digestion of vitamin E is fairly well understood, several pathways regulating net vitamin E absorption remain to be elucidated. In several cell types, cholesterol and vitamin E share common mechanisms for cellular uptake (scavenger receptor B type I and LDL receptors) and efflux (ABCA1 transporters). The role of specific binding proteins in alpha-tocopherol intracellular trafficking is increasingly being understood, leading to new insights into the non-antioxidant functions of vitamin E. SUMMARY: Substantial progress has been made in characterizing the plasma transport of vitamin E and its delivery to cells. Mechanisms regulating the balance between the cellular uptake and efflux of vitamin E are under investigation. Vitamin E is not only an antioxidant but may also modulate pathways of cell signalling and gene expression. The translation of this new knowledge into clinical studies will help define future indications for vitamin E supplementation.     

The effect of dietary vitamin E deficiency on plasma zinc and copper concentrations

Vitamin E and zinc have a number of functions in common, including membrane stabilisation, antioxidant function and modulation of prostaglandin metabolism. Previous studies have shown vitamin E malabsorption during zinc depletion and it appears that there is an interaction between the two nutrients. In this study we have investigated whether vitamin E deficiency affects zinc and copper concentrations in experimental animals. Male Wistar rats were maintained on a vitamin E deficient diet for either 6 or 10 months. At the end of the experimental period all animals had undetectable plasma vitamin E levels and increased red cell fragility. Plasma zinc concentrations were significantly reduced in all vitamin E deficient animals compared to control rats (p<0.002) and copper levels were reciprocally elevated (p<0.002). It appears likely that decreased zinc levels may represent redistribution of circulating zinc to tissues and cells as a secondary antioxidant, or for membrane stabilisation or prostaglandin synthesis.     

Dietary vitamin E supplementation protects the rat large intestine from experimental inflammation

Vitamin E, the most potent antioxidant in the lipid phase, was tested for antiinflammatory activity in trinitrobenzenesulfonic acid-induced rat colitis. Rats were fed a nonpurified diet (saline and control groups) or a vitamin E supplemented diet (treated group, 300 mg/kg nonpurified diet). Vitamin E supplementation, which resulted in increased colonic vitamin E levels, reduced colonic weight and damage score, prevented lipid peroxidation and diarrhea, reduced interleukin-1 beta levels and preserved glutathione reductase activity and total glutathione levels. However, it did not modify myeloperoxidase levels, which are indicative of neutrophil infiltration in the inflamed colon. Vitamin E protects the rat colon from oxidative stress associated with inflammation.