硒与维生素E的协同影响对心肌损伤保护的研究

通过在低硒富锰饲料中联合补充硒及ＶＥ喂养大鼠，并以亚硝酸钠作为诱发因素建立大鼠心肌损伤模型，观察硒与ＶＥ的协同作用对心肌损伤的保护效果。结果表明，在低硒环境下，富锰能显著提高心肌坏死检出率及降低机体抗氧化能力。单纯补充硒及ＶＥ均可对抗富锰的影响，但硒与ＶＥ的联合补充效果更佳。     

氟中毒大鼠心电图改变及其硒的影响

为观察氟中毒大鼠心电图变化及其Ｓｅ的影响，两组Ｗｉｓｔａｒ大鼠饮用１．５８、２．６３ｍｇ／Ｌ高Ｆ＾－水，另两组鼠饮高Ｆ＾－水加饲０．０２５ｍｇ／ｋｇＳｅ饲料，在实验前及实验４、８、１２个月进描记心电图。结果两组大鼠随摄氟时间延长Ｔ波降低，Ｑ－Ｔ间期缩短。     

冠心病病人红细胞变形能力与血浆、红细胞膜硒浓度的关系

目的：从硒与红细胞膜收缩蛋白的关系探讨冠心病病人红细胞变形能力变化的机制。方法：检测１３５例冠心病病人（不稳定性心绞痛４８例，急性心肌梗死５０例，陈旧性心肌梗死３７例）和６６例健康人血浆硒，红细胞膜硒和脂质过氧化物浓度、收缩蛋白二聚体（下简称二聚体）、收缩蛋白四聚体（下简称四聚体）及红细胞变形能力的变化。结果：冠心病病人红细胞滤过指数明显增高，血浆、红细胞膜硒浓度明显降低，与对照组比较有极显著性差异（Ｐ＜０．００１）；冠心病病人红细胞膜脂质过氧化物、二聚体、二聚体与四聚体比值增高，四聚体明显减少，与对照组比较有极显著性差异（Ｐ＜０．００１）。急性心肌梗死病人上述变化均较不稳定性心绞痛和陈旧性心肌梗死病人更明显。冠心病病人红细胞滤过指数与血浆、红细胞膜硒浓度呈负相关（ｒ＝－０．５２４和－０．６６１，Ｐ＜０．００１），红细胞膜硒浓度与脂质过氧化物、二聚体、二聚体与四聚体比值呈负相关（ｒ＝－０．５２１、－０．５７９和－０．５８６，Ｐ＜０．００１），与四聚体呈正相关（ｒ＝０．５５０，Ｐ＜０．００１）。结论：冠心病病人硒缺乏引起的膜骨架结构蛋白异常是红细胞变形能力降低的原因之一。     

高氟摄入后大鼠骨骼肌环核苷酸的变化及镁硒的影响

雄性Ｗｉｓｔａｒ大鼠腹腔ＮａＦ实验表明，亚急性氟中毒大鼠肌骼肌组织环磷酸腺苷（ＣＡＭＰ）水平明显市长中，环磷酸鸟苷（ＣＧＭＰ）水平下降，ＣＡＭＰ／ＣＧＭＰ升高。加镁后，由于ＣＧＭＰ水平升高，使ＣＡＭＰ／ＣＧＭＰ下降，这一作用可能与镁拮抗指一有关。而硒对这一生理过程无明显影响。     

黄绿青霉素对低硒低蛋白大鼠心肌损伤的初步观察

目的 观察黄绿青霉素(CIT)对低硒低蛋白大鼠心肌损伤的特点.方法 40只4周龄Wistar大鼠,雌雄符半,体质量60～80 g,按2×2析因设计随机分为常硒常蛋白无毒素组、常硒常蛋白加毒素组、低硒低蛋白无毒素组和低硒低蛋白加毒素组(将低硒低蛋白合为一种因素考虑),每组10只.分别采用常硒常蛋白和低硒低蛋白饲料喂养大鼠至第10周后,加毒素组大鼠饲料中投予CIT(5 mg·kg-1·d-1)继续喂养至第16周.观察各组大鼠的毛色、摄食、体质量增长情况,计算心脏质量指数,观察心肌病理变化,检测血清硒、白蛋白水平、肌酸激酶(CK)和谷胱甘肽过氧化物酶(GSH-Px)活性以及心肌超氧化物歧化酶(SOD)活性.结果 硒、蛋白和CIT对大鼠体质量、血清硒、白蛋白水平、心脏质量指数、血清CK、GSH-Px活性和心肌SOD活性的影响不存在交互作用(F值分别为0.000、1.210、0.625、0.981、2.785、0.074、0.001,P均>0.05);硒、蛋白对大鼠血清硒、白蛋白水平、心脏质量指数和血清GSH-Px活性的主效应有统计学意义(F值分别为507.698、87.734、4.201、109.389,P均<0.05);CIT对大鼠体质量、血清硒、白蛋白水平、心脏质量指数、血清CK活性的主效应有统计学意义(F值分别为10.929、4.371、26.108、24.844、4.439,P均<0.05).低硒低蛋白两组的血清硒水平[(70.4±40.0)、(87.7 ±59.6)μg/L]低于常硒常蛋A两组[(446.1±74.8)、(502.1±39.2)μg/L,P均<0.05];低硒低蛋白两组的血清白蛋白水平[(34.36±1.28)、(33.38±2.48)g/L]低于常硒常蛋白两组[(40.69±1.30)、(38.71±2.15)g/L,P均<0.05];相同硒和蛋白水平下,加毒素组的心脏质量指数[(4.14±0.36)×10-3、(4.39 ±0.53)×10-3]高于无毒素组[(3.56±0.26)×10-3、(3.80±0.28)×10-3,P均<0.05];低硒低蛋白加毒素组的血清CK活性[(2.54 ±0.56)kU/L]低于低硒低蛋白无毒素组[(3.37±0.67)kU/L,P<0.05].低硒低蛋白两组的血清GSH-Px活性>(408.1±412.6)、(510.5 ±392.0)U/L[低于常硒常蛋白两组[(1667.8±102.2)、(1731.5±144.4)U/L,P均<0.05].电镜结果显示,常硒常蛋白加毒素组大鼠部分心肌细胞闰盘断裂,各带连接断裂,部分区域心肌细胞有溶解现象,有水肿表现;低硒低蛋白无毒素组大鼠心肌细胞膜结构改变不明显,核周围肌丝结构消失,可见大量絮状物质沉积;低硒低蛋白加毒素组大鼠心肌细胞肌节各带结构不很清晰,核旁线粒休嵴轻度疏松,偶见空泡变,大量弥漫性肌质网扩张.结论 CIT是诱导大鼠心肌细胞损伤的主要因素,低硒低蛋白加重病变,但独立致病作用较弱.

Abstract：

Objective To ohserve the rat myocardial damage induced by citreoviridin(CIT)in the status of combined selenium and protein deficiency.Methods According to 2×2 factorial design,forty 4-week-old healthy Wistar rats were randomly divided into four groups.i.e.combined selenium and protein adequate with no CIT and with some CIT groups(Se+Pro+CIT-.Se+Pro+CiT+),combined selenium and protein deficiency with no CIT and with some CIT groups(Se-Pro-CIT-,Se-Pro-CIT+).The numbers of male and female were fifty-fifty.Theserats were fed with combined selenium and protein adequate and combined selenium and protein deficiency fodder until the 16th week. Cardiac toxicity of CIT was evaluated by general state of health, heart weight index, myocardial pathological change, the levels of selenium and the activities of glutathion peroxidase (GSH-Px) and creatine kinase (CK) in serum, and the activity of superoxide dismutase(SOD) of myocardium. Results The interaction effects of combined selenium and protein deficiency and adequate CIT on body weight, serum levels of selenium and albumin, heart weight index, the activities of CK and GSH-Px in serum and SOD of myocardium were statistically not significant(F= 0.000, 1.210, 0.625, 0.981, 2.785, 0.074, 0.001, all P> 0.05). The main effects of combined selenium and protein on the levels of serum selenium and albumin, heart weight index and the activity of GSH-Px in serum were statistically significant(F = 507.698, 87.734, 4.201, 109.389, all P < 0.05). The main effects of CIT on body weight, the levels of serum selenium and albumin, heart weight index and the activity of CK in serum were statistically significant(F = 10.929, 4.371, 26.108, 24.844, 4.439, all P < 0.05). The mean levels of serum selenium of Se-Pro- groups [(70.4 ± 40.0), (87.7 ± 59.6 )μg/L] were lower than those of Se+Pro+ groups [(446.1 ± 74.8),(502.1 ± 39.2)μg/L, all P < 0.05]. The mean levels of serum albumin of Se-Pro- groups [(34.36 ± 1.28 ), (33.38 ±2.48)g/L] were lower than those of Se+Pro+ groups[(40.69 ± 1.30), (38.71 ± 2.15)g/L, all P < 0.05]. The mean levels of heart weight index of CIT+ groups[(4.14 ± 0.36) × 10-3, (4.39 ± 0.53) x 10-3] were higher than those of CIT-groups[(3.56 ± 0.26) x 10-3, (3.80 ± 0.28) x 10-3, all P < 0.05] respectively at the same levels of selenium and protein. The mean levels of CK in serum of Se-Pro-CIT+ group[(2.54 ± 0.56)kU/L] was lower than that of Se-Pro-CIT- group [(3.37 ± 0.67 )kU/L, P < 0.05]. The mean levels of activity of GSH-Px in serum of Se-Progroups[(408.1 ± 412.6), (510.5 ± 392.0)U/L] were lower than those of Se+Pro+ groups[(1667.8 ± 102.2),(1731.5 ± 144.4)U/L, all P < 0.05]. In Se+Pro+CIT+ group, there was part of intercalary disc of cardiac myocytes fragmented;the conjunctions between myoeytes were broken;in some region, cardiac myocytes became edematous,even dissolved. In Se-Pro-CIT- group, the change of cardiac myocytes membrane structures was not obvious;filament structure was disappeared around nucleus;deposition of mass floccule could be seen. In Se-Pro-CIT+ group,the structure of sarcomeres was not obvious;mitochondrial cristae was loosened;cavities in myocytes could be seen occasionally;there were lots of disseminated sareoplasmic reticulum extending. Conclusions .CIT is the main risk factor in inducing myocardial damage. The deficiency of combined selenium and protein can aggravate the damage,but its independent pathogenic effect is weak.     

The Association of Measures of the Micro- and Macro-Vasculature with Selenium and GPx Activity in a Young Bi-Ethnic Population: The African-PREDICT Study

Abstract

Objective: Selenium plays an important physiological role as component for antioxidant selenoproteins such as glutathione peroxidase (GPx). Since oxidative stress contributes to hypertension development, it is likely that selenium deficiency may contribute to the burden of cardiovascular disease. To better understand the involvement of selenium and GPx in the early development of cardiovascular disease, we investigated in young, healthy black and white African men and women whether measures of the micro- and macrovasculature are related to selenium and GPx activity.

Methods: In young adults (N?=?394; aged 20–30?years) we determined serum selenium, GPx activity, microvascular measures (central retinal artery equivalent, central retinal vein equivalent, arteriolar-to-venular ratio [AVR], and estimated glomerular filtration rate [eGFR]), and macrovascular measures (pulse wave velocity, 24-hour pulse pressure [PP] and augmentation index [Aix]).

Results: In multivariable-adjusted regression analyses, there were vasculoprotective associations between serum selenium and a microvascular measure (AVR [β?=?0.23; p?=?0.036]) in black African women and with a macrovascular measure (24-hour PP [β = ?0.15; p?=?0.048]) in white African women. In turn, GPx activity also showed a protective association with a microvascular measure (eGFR) in white African men (β?=?0.23; p?=?0.035), as well as with macrovascular measures (AIx, PP) in the black (β = ?0.25; p?=?0.027) and white African men (β = ?0.22; p?=?0.035), and black African women (β = ?0.32; p?=?0.001).

Conclusions: Collectively the findings suggest a protective role for the micronutrient selenium and GPx on both the micro- and macrovasculature in a young, healthy bi-ethnic population.     

Toxicity of 3′3-ditrifluormethyldiphenyl diselenide administered during intra-uterine development of rats

The aim of this study was to assess the effects of the organoselenium compound, 3′3-ditrifluormethyldiphenyl diselenide [(F₃CPhSe)₂], during the intra-uterine development of Wistar rats. Dams were given repeated doses of 1, 5 or 10 mg/kg (F₃CPhSe)₂ by intragastric route on gestation days 6–15, and cesarean sections were performed on day 20 of pregnancy. The numbers of implantation sites, living and dead fetuses and resorptions were recorded. Fetuses were weighed and stained with Alizarin red S for skeletal evaluation. The placental morphology was also evaluated. In 1 mg/kg (F₃CPhSe)₂ group, neither maternal toxicity nor prenatal growth retardation was observed. Conversely, in 5 and 10 mg/kg groups, there was a decrease in maternal weight gain during pregnancy indicating that (F₃CPhSe)₂ was maternally toxic, without affecting fetuses weight and length. (F₃CPhSe)₂ caused some morphological alterations in placenta of 5 and 10 mg/kg-exposed dams. Results also showed that skeletal variations were produced by (F₃CPhSe)₂ only at doses (10 mg/kg) in which a marked embryolethality was found. We conclude that (F₃CPhSe)₂ was toxic to the dams and induced embryofeto-toxicity at doses equal to 10 mg/kg.     

硒与高危妊娠病理生理的关系

硒(Se)是人体必需的微量矿物质,对妊娠有着极其重要的作用。Se是含硒蛋白的一个组分,有维持酶蛋白催化功能的作用。Se缺乏可诱发妊娠高血压疾病,妊娠肝内胆汁淤积症,胎儿宫内发育迟缓,羊水过少,胎膜早破等高危妊娠的发生。增加硒摄入可降低高危妊娠的危险度。     

Diphenyl diselenide protects rat hippocampal slices submitted to oxygen-glucose deprivation and diminishes inducible nitric oxide synthase immunocontent

Diphenyl diselenide (PhSe)2 is an organic selenium compound that has been little studied. In this study we investigated the effects of (PhSe)2 (0.1-3 microM) in a classical model of in vitro brain ischemia, which consists of exposing rat hippocampal slices to oxygen-glucose deprivation (OGD). Hippocampal slices were exposed for 60 min to OGD and the cellular viability (performed by MTT assay) as well as the immunocontent of nitric oxide synthase inducible (iNOS) were evaluated after 180 min of a recovery period. OGD decreased cellular viability by 50% and increased more than twice the immunocontent of iNOS of hippocampal slices. (PhSe)2 (1 and 3 microM) added during OGD and the recovery period abolished both effects. These results demonstrate for the first time the neuroprotective effects of (PhSe)2. Although the selenium analog--ebselen--has been widely used in ischemia models, our results suggest that other selenoorganic compounds could be investigated as pharmacological tools against brain disorders.     

富硒康治疗消化性溃疡

目的:探讨富硒康口服液治疗消化性溃疡病的临床意义。方法:采用双盲对照法,治疗组:富硒康+雷尼替丁;对照组:雷尼替丁。结果:治疗组溃疡愈合率明显高于对照组(P<0.01),胃溃疡显效率为83.3%;十二指肠溃疡显效率为88.8%。结论:富硒康与H2受体拮抗剂对治疗消化性溃疡病有协同作用,它既有治疗用途,同时又起保健作用。