1,25-二羟维生素D_3对人癌实体瘤的异种移植瘤体内生长的抑制

已证明几种人类癌细胞株有1,25-二羟维生素D_3(1,25-(OH)_2D_3)的特异性高亲和力受体。1,25-(OH)_2D_3及其代谢物在体外能够抑制人类乳腺癌和恶性黑素瘤细胞株生长,并且1,25-(OH)_2D_3及其一种人工合成类似物能够延长用白血病细胞接种的白血病小鼠的存活期。本文研究了1,25-(OH)_2D_3及其同类物在小鼠体内对人类肿瘤的三个细胞株的异种移植瘤生长的抑制作用。 CBA/Lac小鼠出生后16～18天时切除胸腺,饲养18～21天后,经腹腔注射1-β-D阿糖呋喃嘧啶200mg/kg,48小时后用~(137)Csr射线     

1,25-二羟维生素D_3对β淀粉样蛋白1-42诱导PC12细胞焦亡的保护作用

目的探讨1,25-二羟维生素D_3[1,25(OH)_2D_3]对β淀粉样蛋白1-42(Aβ_(1-42))诱导的PC12细胞焦亡的保护作用。方法 Aβ_(1-42)诱导PC12细胞构建体外阿尔茨海默病(Alzheimer’s disease, AD)细胞模型,设立对照组、模型组(20μmol/L Aβ_(1-42))及不同浓度1,25(OH)_2D_3预处理组[1、10、100 nmol/L 1,25(OH)_2D_3+20μmol/L Aβ_(1-42)]。CCK-8检测1,25(OH)_2D_3对Aβ_(1-42)诱导的PC12细胞活性,吖啶橙/溴乙锭(AO/EB)染色检测细胞膜通透性,比色法、酶联免疫吸附法检测乳酸脱氢酶(lactic dehydrogenase, LDH)和白细胞介素1β(interleukin-1β,IL-1β)水平,免疫蛋白印迹法检测NOD样受体家族蛋白(NOD-like receptor family protein 1, NLRP1)、含半胱氨酸的天冬氨酸蛋白水解酶-1(cysteinyl aspartate specific proteinase-1, caspase-1)和消皮素D(gasdermin D, GSDMD)蛋白表达。结果与对照组相比,模型组细胞活性显著降低(P0.01),细胞膜通透性、LDH、IL-1β、NLRP1、caspase-1和GSDMD蛋白显著升高(P0.01)。与模型组相比,3个1,25(OH)_2D_3预处理组的细胞活性均有所提高(P0.05),细胞膜破损减少。10和100 nmol/L 1,25(OH)_2D_3预处理组细胞LDH释放、IL-1β水平显著降低(P0.01)。1 nmol/L 1,25(OH)_2D_3组中NLRP1和GSDMD蛋白的表达量明显降低(P0.05),10和100 nmol/L 1,25(OH)_2D_3组降低更为显著(P0.01),10和100 nmol/L 1,25(OH)_2D_3组的caspase-1蛋白表达显著降低(P0.05,P0.01)。结论 1,25(OH)_2D_3对Aβ_(1-42)诱导的PC12细胞焦亡具有保护作用。     

维生素C和维生素D_3水平对女性抗氧化能力影响

目的探讨血清维生素C(VC)和维生素D_3(VD_3)水平对女性抗氧化能力的影响。方法集中收集2017年1—2月在山西省太原市山西民盛体检中心体检的124名25～45岁健康女性的血清样本,采用高效液相色谱–紫外检测法检测VC含量,根据VC水平将其分为高VC组(≥2μg/mL)和低VC组(2μg/mL),采用酶联免疫吸附法检测25–羟基维生素D_3[25-(OH)D_3]和1,25–二羟基维生素D_3[1,25-(OH)_2D_3)含量,采用比色法检测超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,比较高VC组与低VC组的差异;对25-(OH)D_3水平30 ng/mL且同意参与补充VD_3的65人(均为高VC组)进行干预,2017年4月6日收集其血清,比较干预前后25-(OH)D_3、1,25-(OH)_2D_3、SOD和GSH-Px水平的变化。结果高VC组血清25-(OH)D_3含量为(22.65±5.51)ng/mL,1,25-(OH)_2D_3含量为(19.10±5.60) pg/mL, SOD活性为(79.25±26.98) U/mL, GSH-Px活性为(32.73±6.06) nmol/mL,均高于低VC组,除25-(OH)D_3外,差异均有统计学意义(P 0.05)。VC与1,25-(OH)_2D_3、SOD及GSH-Px呈正相关,25-(OH)D_3与1,25-(OH)_2D_3呈正相关,1,25-(OH)_2 D_3与SOD呈正相关。补充VD_3后血清25-(OH)D_3含量为(40.66±12.12)ng/mL,1,25-(OH)_2D_3含量为(24.79±4.93)pg/mL,SOD活性为(86.05±26.95)U/mL,GSH-Px活性为(42.11±8.22)nmol/mL,均高于补充VD_3前,且差异均有统计学意义(P 0.05)。结论在一定范围内VC能够促进VD_3活化为1,25-(OH)_2D_3,VC和VD_3能够降低机体的氧化应激水平,提高抗氧化能力。     

镉对小鸡25-羟基胆骨化醇代谢的影响

1,25-二羟基胆骨化醇(1,25-DHGG)是维生素D_3在肾脏中形成的代谢物,也是这种维生素的代谢起作用的形式。过去的实验证明镉能降低肾脏中某些酶的活性,因此作者企图观察肾脏中合成1,25-     

血清1,25-二羟维生素D3水平对老年骨质疏松症患者骨骼肌减少症的预测价值

目的探讨血清1,25-二羟维生素D3〔1,25-(OH)_2D_3〕水平对老年骨质疏松症(OP)患者骨骼肌减少症(SAR)的预测价值。方法选取2015年3月-2018年3月我院收治的OP患者246例为研究对象,回顾性分析一般临床资料,根据OP是否合并SAR分为合并SAR组(n=180)和未合并SAR组(n=66),分析患者血清1,25-(OH)_2D_3水平与OP合并SAR的相关性,进一步探讨预测价值。结果合并SAR组血清1,25-(OH)_2D_3、钙(Ca)、碱性磷酸酶(ALP)水平显著低于未合并SAR组,ALT高于未合并SAR组(P0.05),但两组GLU水平比较无明显差异(P0.05); Spearman秩相关性分析发现OP患者血清1,25-(OH)2D3水平与ASMI不相关(P0.05),与握力、步速呈正相关(P0.05); OP患者血清1,25-(OH)2D3水平与胰岛素抵抗指数(HOMA-IR)、体质量(BMI)、超敏C反应蛋白(hs-CRP)不相关(P0.05),与雌二醇(E2)、睾酮(T)、白介素-10(IL-10)、胰岛素样生长因子-1(IGF-1)水平呈正相关(P0.05),与活性氧(ROS)、全段甲状旁腺素(i PTH)、肿瘤坏死因子(TNF-α)、白介素-6(IL-6)呈负相关(P0.05)。结论血清1,25-(OH)_2D_3水平在是否合并SAR的OP患者中存在显著差异,且还与OP患者SAR部分评价指标及影响因素相关,在OP合并SAR中有一定预测价值。     

哮喘患儿血清1,25-二羟维生素D3和IL-25与肺功能及生活质量的相关性研究

目的探讨哮喘患儿血清1,25-二羟维生素D3[1,25(OH)_2D_3]水平和白介素-25(IL-25)的水平与肺功能和生活质量的关系。方法选取该院2013年11月-2014年12月急性期哮喘患儿30例(观察组)和同期健康患儿30例(对照组)为研究对象,取空腹静脉血,采用酶联免疫分析(ELISA)法测定血清中1,25(OH)_2D_3和IL-25的浓度,并对哮喘患儿进行肺功能检查及用儿童哮喘患者生活质量调查问卷(PAQLQ)进行生活质量评分。结果观察组患儿血清1,25(OH)_2D_3显著低于对照组,IL-25水平均显著高于对照组,PAQLQ分值明显低于对照组,观察组患儿血清IL-25均与肺功能指标FEVl%、FEVl/FVC%呈负相关(r=-0.493,P0.05;r=-0.485,P0.05)和PAQLQ分值均呈负相关(r=-0.341,P0.05;r=-0.503,P0.05;r=-0.476,P0.05),1,25(OH)_2D_3与肺功能指标FEVl%、FEVl/FVC%呈正相关(r=0.513,P0.05;r=0.504,P0.05)和PAQLQ分值均呈正相关(r=0.389,P0.05;r=0.532,P0.05;r=0.587,P0.05);PAQLQ分值均与肺功能呈正相关。结论血清1,25(OH)_2D_3和IL-25参与了哮喘的急性反应,可作为判断哮喘急性期指标;哮喘患儿的肺功能和生活质量下降可能与两者有关。     

1,25二羟维生素D3对肝癌HepG2细胞增殖侵袭影响

目的探讨1,25二羟维生素D3[1,25(OH)_2D_3]及PI3K/AKT信号通路抑制剂(LY294002)对人肝癌Hep G2细胞的增殖、侵袭影响及作用机制。方法实验设10~(-8)、10~(-7)、10~(-6)mol/L 1,25(OH)_2D_3组及2.5、5.0、10.0、20.0、40.0、80.0μmol/L LY294002组,10~(-7)mol/L 1,25(OH)_2D_3+5μmol/L LY294002联合组,噻唑蓝法检测人肝癌Hep G2细胞增殖抑制率;Compu Syn软件计算联合指数;Tanswell小室检测HepG2细胞侵袭数;Western blot检测Hep G2细胞增殖细胞核抗原(PCNA),细胞基质金属蛋白酶9(MMP-9)、磷酸化丝氨酸苏氨酸蛋白激酶(p-AKT)、10号染色体缺失且与张力蛋白同源物磷酸脂酶基因(PTEN)蛋白。结果 1,25(OH)_2D_3及LY294002对人肝癌HepG2细胞增殖抑制率呈时间-剂量依赖效应(P0.05);1,25(OH)2D3联合LY294002组细胞增殖抑制率明显高于二者单独处理组(P0.05),联合指数=0.728,2者具有协同效应;10-7mol/L 1,25(OH)2D3组、5μmol/L LY294002组以及联合组Hep G2细胞侵袭数[分别为(45.9±6.4)、(49.9±6.0)、(27.8±4.0)个]明显低于对照组[(64.6±8.0)个](P0.05)。与对照组比较,10-7mol/L 1,25(OH)2D3组及联合组HepG2细胞PTEN蛋白表达量增加,差异有统计学意义(P0.05),10-7mol/L 1,25(OH)_2D_3组、5μmol/L LY294002组及联合组HepG2细胞PCNA、MMP-9、p-AKT蛋白表达均降低,差异有统计学意义(P0.05),且联合组蛋白表达量低于二者单独处理组(P0.05)。结论 1,25(OH)_2D_3可抑制人肝癌HepG2细胞增殖、侵袭,其机制可能与上调PTEN表达,抑制PI3K/AKT信号通路活性,下调PCNA、M M P-9蛋白有关;与LY294002合用具有协同效应。     

维生素D受体与肿瘤的研究进展

维生素D受体(Vitamin Dreceptor VDR)属于类固醇激素,能介导1,25(OH)2D3(1,25-二羟胆骨化醇1,25-dihydroxyc-holecalciferol)调节多种正常组织或肿瘤组织细胞的生长和分化。VDR基因上存在多个多态性位点,与部分肿瘤的发生发展密切相关。本文主要介绍了VDR的结构和功能、生物学效应、作用机制以及VDR基因多态性与一些肿瘤的相关性研究。     

1α-羟基维生素D_3和1,25-二羟基维生素D_3对人体无机盐代谢的作用 Ⅰ.对磷的净吸收影响

维生素D(V_D)固醇对人体肠吸收磷的影响尚未被广泛地研究,这是由于放射性磷的应用受到限制,而影响了用代谢平衡方法对这一问题的观察。本文作者描述了1,25-(OH)_2D_3(1,25-二羟基维生素D_3)或1α(OH)D_3(1α-羟基维生素D_3)对患有进行期肾衰竭病人和正常人对磷净吸收的影响。     

1,25—二羟维生素D3对基因表达的调控

自70年代初发现了活性维生素 D(Calcitr-iol,1,25-二羟胆钙化醇)受体(VDR)后,有关1,25-(OH)_2-D_3的生物活性,VDR 结构及功能的研究取得了飞速的进展。已证实 VDR广泛分布于肠道、骨组织、肾脏,单核—巨噬细胞、激活的淋巴细胞,以及某些肿瘤细胞;1,25-(OH)_2-D_3和 VDR 有高度亲合力(KD=1～50×10~(-11)M),形成的复合物通过与靶基因相互作用,影响钙,磷代谢,骨质形成,某     

Comparison of 26,27-hexafluoro-1 alpha,25-dihydroxyvitamin D3 and 1 alpha,25-dihydroxyvitamin D3 on the resorption of bone explants ex vivo.

26,27-Hexafluoro-1 alpha,25-dihydroxyvitamin D3 [F6-1,25-(OH)2D3] is more potent than 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] in stimulating bone resorption in vitro and in vivo. The reason why F6-1,25(OH)2D3 is more active remains unclear. To clarify the relationship between the bone-resorbing activity of each vitamin D3 analogue and the metabolism of each analogue, in the present study, we used an ex vivo method that was established by Reynolds et al (Calcif Tissue Res, 1974, 15, 333-339). The effect of F6-1,25(OH)2D3 or 1,25(OH)2D3 on 45Ca release from parietal bones, prepared at 3, 14 and 24 h after injection of 1.9, 3.8, 7.6 or 15.2 pmol vitamin D analog/g body weight, was examined. F6-1,25(OH)2D3 was more potent than 1,25(OH)2D3 during each in vivo time period. 1,25(OH)2D3 at 3 h after the injection was more active compared to the control (no injection of 1,25(OH)2D3) but not at 14 and 24 h. The radioactivity of the bones after the injection of [3H]-F6-1,25(OH)2D3 was retained even at 24 h. In the case of [3H]-1,25(OH)2D3, the radioactivity of bones decreased with an increase in the in vivo period. In a HPLC analysis of the lipid extract of bone homogenate, [3H]-F6-1,25(OH)2D3 alone was detected at 3 h after the injection and both [3H]-F6-1,25(OH)2D3 and [3H]-26,27-hexafluoro-1 alpha, 23S,25-trihydroxyvitamin D3 [F6-1,23,25(OH)3D3] were detected at 14 and 24 h after the injection. [3H]-1,25(OH)2D3 was highly detected at 3 h after the injection, but it decreased with an increase in the in vivo period. In the ex vivo test, the activity of F6-1,23,25(OH)3D3 was less than that of F6-1,25(OH)2D3 but similar to that of 1,25(OH)2D3. The present study indicates that F6-1,25(OH)2D3 is more active and more long-lasting than 1,25(OH)2D3 in the ex vivo method. A higher potency of F6-1,25(OH)2D3 is explained, at least partly, by the results that the amounts of both F6-1,25(OH)2D3 and its active metabolite, F6-1,23,25(OH)3D3, in the bones are higher than that of 1,25(OH)2D3, and that F6-1,25(OH)2D3 and its metabolite are retained in bones longer than 1,25(OH)2D3.     

Dietary phosphate deprivation increases renal synthesis and decreases renal catabolism of 1,25-dihydroxycholecalciferol in guinea pigs.

In guinea pigs, dietary phosphate deprivation decreases plasma phosphate concentration, increases plasma 1.25-dihydroxycholecalciferol [1,25-(OH)2D3] concentration and causes hypercalcemia concurrent with the maximal increase in plasma 1,25-(OH)2D3 levels. Our objective was to determine whether increased synthesis or decreased catabolism contributed to the elevation in plasma 1,25-(OH)2D3. Preliminary experiments using renal mitochondria from guinea pigs fed a control diet revealed that 23,25-dihydroxycholecalciferol [23,25-(OH)2D3], not 24,25-dihydroxycholecalciferol [24,25-(OH)2D3], was the reciprocal side-chain metabolite to 1,25-(OH)2D3 in this species. An assay employing guinea pig renal mitochondria was used to measure the renal synthesis of 1,25-(OH)2D3 and 23,25-(OH)2D3 from [3H]25-OH-D3. These metabolites were unequivocally identified by combinations of HPLC, ultraviolet spectrophotometry and mass spectrometry. This renal mitochondrial assay was subsequently used to investigate the effect of dietary phosphate deprivation on guinea pig vitamin D metabolism. Within 1 wk the rate of synthesis of 1,25-(OH)2D3 was maximal in phosphate-deprived guinea pigs. This rate was significantly (P less than 0.005) higher than that achieved in same-day control guinea pigs. Conversely, within 1 d the synthesis of 23,25-(OH)2D3 was significantly (P less than 0.005) decreased in phosphate-deprived guinea pigs. Similarly, the rate of 1,25-(OH)2D3 metabolism was decreased within 1 d of dietary phosphate deprivation and was at a minimum within 1 wk. This rate was significantly (P less than 0.005) less than that attained in same-day control guinea pigs. These results suggest that both increased synthesis and decreased metabolism of 1,25-(OH)2D3 contribute to the plasma 1,25-(OH)2D3 elevation that occurs in response to dietary phosphate deprivation.     

Efficacy of several vitamin D compounds in the prevention of tibial dyschondroplasia in broiler chickens

Studies were conducted to evaluate several cholecalciferol (D3 metabolites: 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], 1,24R,25-trihydroxycholecalciferol [1,24R,25-(OH)3D3], 1 alpha-hydroxy-cholecalciferol (1 alpha-OHD3), 24R,25-dihydroxycholecalciferol [24R,25-(OH)2D3], 1,25-dihydroxy-26,27 hexadeuterium cholecalciferol (1,25-(OH)2-26,27[2H]6D3) and 1,25-dihydroxy-24R-fluorocholecalciferol [1,25-(OH)2-24R-FD3] for their activity in preventing the development of tibial dyschondroplasia in broilers. The basal diet used is low in calcium, high in phosphorus and chlorine and is known to promote a high incidence of tibial dyschondroplasia. The chicks received ultraviolet radiation from fluorescent lights in addition to 1100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet. Supplementation of the diet with 10 micrograms/kg of all the metabolites except 24R,25-(OH)2D3 significantly lowered the incidence and severity of tibial dyschondroplasia and increased bone ash when compared to birds receiving the basal diet. None of the active D3 metabolites was effective when fed at 0.1 or 1.0 micrograms/kg of diet. Two active compounds tested [1,25-(OH)2D3 and 1,24R,25-(OH)3D3] at 5 micrograms/kg of diet were effective in reducing either the incidence or severity of tibial dyschondroplasia.     

25-Hydroxyvitamin D and 1,25-dihydroxyvitamin D of D2 and D3 origin in maternal and umbilical cord serum after vitamin D2 supplementation in human pregnancy

Serum concentrations of 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] of vitamin D2 and D3 origin were determined separately in 10 women before vitamin intake in early pregnancy, and repeated in maternal and cord serum obtained at delivery after 20 to 30 wk of vitamin D2 supplementation in a dose of 400 IU/day. Before supplementation 25-OHD2 and 1,25-(OH)D2D2 were present in just traceable or nondetectable concentrations, but the levels increased in all to a mean +/- 1 SD of 7.3 +/- 3.7 ng/ml and 37.2 +/- 18.1 pg/ml, respectively (p less than 0.0025), by the time of delivery. At delivery the total 25-OHD and 1,25-(OH)2D levels were always lower in the cord than in the maternal serum (30.7 +/- 14.2 versus 20.1 +/- 9.1 ng/ml, and 90.1 +/- 31.2 versus 37.3 +/- 11.6 pg/ml, p less than 0.0025). The paired concentrations of 25-OHD were closely related (r = 0.89, p less than 0.0005), while the association for 1,25-(OH)2D was not statistically significant (r = 0.53, p less than .01). The 25-OHD of D2 and D3 origin accounted for a similar proportion of the total 25-OHD in the maternal and cord serum (ratio of 25-OHD2 to 25-OHD3: 0.40 +/- 0.28 versus 0.45 +/- 0.29, p = NS), as did the respective 1,25-(OH)2D metabolites [ratio of 1,25-(OH)2D2 to 1,25-(OH)2D3: 0.73 +/- 0.35 versus 0.90 +/- 0.50, p = NS].(ABSTRACT TRUNCATED AT 250 WORDS)     

Diabetes prevalence is associated with serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in US middle-aged Caucasian men and women: a cross-sectional analysis within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial

Hypovitaminosis D may be associated with diabetes, hypertension and CHD. However, because studies examining the associations of all three chronic conditions with circulating 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) are limited, we examined these associations in the US Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial (n 2465). Caucasian PLCO participants selected as controls in previous nested case-control studies of 25(OH)D and 1,25(OH)(2)D were included in this analysis. Diabetes, CHD and hypertension prevalence, risk factors for these conditions and intake of vitamin D and Ca were collected from a baseline questionnaire. Results indicated that serum levels of 25(OH)D were low (< 50 nmol/l) in 29 % and very low (< 37 nmol/l) in 11 % of subjects. The prevalence of diabetes, hypertension and CHD was 7, 30 and 10 %, respectively. After adjustment for confounding by sex, geographical location, educational level, smoking history, BMI, physical activity, total dietary energy and vitamin D and Ca intake, only diabetes was significantly associated with lower 25(OH)D and 1,25(OH)(2)D levels. Caucasians who had 25(OH)D ≥ 80 nmol/l were half as likely to have diabetes (OR 0·5 (95 % CI 0·3, 0·9)) compared with those who had 25(OH)D < 37 nmol/l. Those in the highest quartile of 1,25(OH)(2)D (≥ 103 pmol/l) were less than half as likely to have diabetes (OR 0·3 (95 % CI 0·1, 0·7)) than those in the lowest quartile (< 72 pmol/l). In conclusion, the independent associations of 25(OH)D and 1,25(OH)(2)D with diabetes prevalence in a large population are new findings, and thus warrant confirmation in larger, prospective studies.     

Vitamin D status and parathyroid hormone concentrations in Chinese women and men from north-east of the People's Republic of China

STUDY OBJECTIVE: To evaluate vitamin D status of young and old women and men living in Shenyang, north-east People's Republic of China in early spring and to explore the relationship between vitamin D metabolites and parathyroid hormone (PTH) in this population. DESIGN: Cross-sectional study. SETTING: Shenyang, north-east China. SUBJECTS: 194 healthy volunteers: 48 young women and 48 young men aged 25-35 y, and 48 old women and 50 old men aged 65-75 y. RESULTS: Fasting blood samples were used to measure plasma 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D) and PTH using radioimmunoassays. The proportion of subjects who could be regarded as vitamin D deficient (<25 nmol/l) was 48%, 29%, 15% and 13% for old men, young men, old women and young women, respectively. There was no association between plasma 1,25(OH)2D and 25(OH)D concentrations. PTH concentrations were elevated in both old women and men compared with young subjects (P<0.01). A negative association between PTH and 25(OH)D was only found in old women (P<0. 001), but not in old men, nor in young subjects. CONCLUSIONS: Vitamin D status was poor in this population in early spring, especially in men. There was no clear evidence to show that the secretion of PTH and the conversion of 1,25(OH)2D were affected by the low 25(OH)D concentration. SPONSORSHIP: Partly supported by the Sandoz Foundation for Gerontological Research and the Nestlé Foundation, Switzerland, and Medical Research Council, UK. European Journal of Clinical Nutrition (2000) 54, 68-72     

All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats

An antagonistic interaction between retinol and calciferol has been established. However, the mechanism by which this antagonism occurs is unclear. One possibility is that retinol affects the metabolism of calciferol. To investigate this hypothesis, retinol- and calciferol-depleted rats were given various amounts of ergocalciferol, cholecalciferol, 1alpha,25-dihydroxycholecalciferol [1,25(OH)2D3], or 24,24-difluoro-1alpha,25-dihydroxycholecalciferol [24-F2-1,25(OH)2D3] in combination with various amounts of retinyl acetate or all-trans retinoic acid (ATRA) in a series of studies. Rats administered 1720 or 3440 microg retinyl acetate once every 3 d for 33 d in combination with 25.8 ng ergocalciferol or 25 ng cholecalciferol every 3 d had lower serum calcium and greater serum phosphorus concentrations than rats fed 0 or 11.4 mug retinyl acetate every 3 d. In addition, rats fed 400 microg ATRA/d in combination with 25.8 ng ergocalciferol every 3 d, 25 ng cholecalciferol every 3 d, 2-5 ng 1,25(OH)2D3/d, or 0.5-1 ng 24-F2-1,25(OH)2D3/d had significantly lower serum calcium and higher serum phosphorus concentrations than rats not given ATRA in the diet. Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol and cholecalciferol in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated. Together, these results suggest that retinol does not antagonize the action of calciferol by altering the metabolism of calciferol or 1,25(OH)2D3, but does so by another mechanism.     

老年妇女PTH分泌异常及1，25（OH）2D3的疗效观察

目的 研究老年妇女甲状旁腺激素的分泌变化以及维生素1，25(OH)2D3的疗效。方法测定20例年轻妇女(25～35岁)和20例老年妇女(70～78岁)血清PTH浓度，用RIA方法测定使用1，25(OH)2D3前后VFH的变化。使用RIA方法测定血清1，25(OH)2D和25(OH)D的血清浓度。结果 血清PTH浓度随增龄而升高，使用1，25(OH)2D3后，两组的PTH水平均下降。结论 1，25(OH)2D3能减少老年妇女PTH分泌的异常增加。