硒、锰对大鼠全血及组织中硒、锰水平以及谷胱甘肽过氧化物酶活性的影响

本文以干酪素及蔗糖作主要成分构成合成饲料,观察饲料中不同水平的硒、锰含量对大鼠体内硒、锰水平及谷胱甘肽过氧化物酶活性的影响。实验结果表明,低硒组的全血、心肌、肝脏、肾及毛中的硒含量均显著低于常硒组。全血、心肌及肝脏的GSH-Px活性也明显受饲料硒含量的影响。值得注意的是喂富锰饲料的大鼠其全血、肝脏及心肌锰含量与常锰组相当,因此,饲料锰含量对大鼠组织硒含量及GSH-Px活性也无明显的影响。提示锰对大鼠体内硒含量及GSH-Px活性的影响是复杂的,它可能受到饲料组成及饲料中蛋白质含量的明显影响。     

孕中期弓形虫感染对孕鼠血清孕酮及雌三醇含量的影响

目的探讨孕中期弓形虫感染对孕鼠血清孕酮(progesterone)及雌三醇(estriol)含量的影响。方法孕中期BALB/c孕鼠随机分为染虫组和健康对照组,染虫组经腹腔无菌接种纯化的RH强毒株弓形虫速殖子,健康对照组注射等量0.01mol/LPBS。分别于妊娠第10、12、14、16、18d,摘孕鼠眼球取血,经放射免疫法测定血清孕酮和雌三醇含量。结果在孕第10、12、14d,孕鼠血清孕酮和雌三醇含量染虫组与对照组比较差异无统计学意义(P>0.05);在孕第16、18d,两组比较差异有统计学意义(P<0.01)。结论孕中期弓形虫感染可引起孕鼠血清孕酮和雌三醇含量下降,这可能是弓形虫感染致胚胎发育迟缓、胎盘组织炎性病变及滋养层细胞凋亡增加的结果,也可能是胚胎发育迟缓、滋养层细胞凋亡增加的原因。     

孕鼠感染弓形虫对子代的影响

目的观察孕期感染弓形虫对子代鼠发育、寿命和免疫功能的影响。方法以不同剂量RH株弓形虫腹腔感染孕中期鼠(d10),分娩后观察记录子鼠发育过程中体长、体重、寿命;给予实验目的要求的干预措施,观察智力发育情况及免疫功能变化。结果弓形虫轻感组、重感组、对照组孕鼠分娩子鼠体长差异无显著性,体重、寿命、智力发育有差别;重感组子鼠寿命明显短于对照组和轻感组。轻感组子鼠智力干预前后差异有显著性,子鼠智力可以通过干预措施达到正常或得到改善,其他组无明显变化;受到再攻击感染时,重感染组子鼠感染率显著高于轻感组和对照组,且与IgG含量成反比。孕期弓形虫重度感染使子鼠抗感染能力下降,但血清特异性抗体IgG能起到一定的保护作用。结论孕期感染弓形虫出生子鼠体重、智力、免疫功能降低,寿命缩短,与感染剂量大小有关。对体长无明显影响。     

MSeC对鸡胚肝脏和脑组织中谷胱甘肽过氧化物酶和脱碘酶活性的影响

目的通过补硒对正常鸡胚脑和肝脏中谷胱甘肽过氧化物酶(GPx)和脱碘酶活性的影响,探讨补硒对于正常动物的影响。方法对孵育8d的鸡胚注射不同剂量的甲基硒代半胱氨酸(MSeC),含硒量分别为0、1、5、10、20μg,第20天时测定脑组织和肝脏中硒水平、GPx活性及脱碘酶活性。结果对正常鸡胚补硒,可有效提高脑和肝脏的硒水平及GPx活性,还可提高肝脏Ⅰ型脱碘酶(IDⅠ)活性,但对脑中Ⅱ型脱碘酶(IDⅡ)活性没有影响。补硒量与除脑IDⅡ活性外的其他指标都显著相关(P<0.01)。结论MSeC是一个有效的补硒制剂,对于正常鸡胚,补硒可提高肝脏、脑组织硒水平和肝GPx、IDⅠ活性及脑GPx活性,其补硒效应有随补硒量增加而增强的趋势。     

弓形虫感染对妊娠中期孕鼠血清中胎盘激素含量的影响

目的探讨妊娠中期弓形虫感染对BALB/c孕鼠血清绒毛膜促性腺激素（CG）、胎盘催乳素（PL）和雌三醇（E3）含量的影响。方法在妊娠第8 d,采用腹腔注射法建立弓形虫感染的BALB/c小鼠动物模型,于妊娠第12、14、16、18d分批摘眼球取血,处死孕鼠,采用放射免疫分析法（RIA）测定孕鼠血清CG、PL和E3含量。结果实验组和正常对照组孕鼠血清CG含量均随妊娠天数的增加而降低,PL和E3含量均随妊娠天数的增加而升高（CG：F对照组=19.306,F实验组=57.620;PL：F对照组=17.449,F实验组=46.720;E3：F对照组=239.546,F实验组=22.841,P均〈0.01）;妊娠第16 d和第18 d时3种激素含量实验组与正常对照组比较差异有统计学意义（CG：t16=4.351,t18=13.367;PL：t16=4.034,t18=2.875;E3：t16=4.265,t18=11.499,P均〈0.01）。结论妊娠中期弓形虫感染孕鼠血清中胎盘激素含量较正常对照组显著降低,这可能是虫体感染所致的胎盘组织病理损伤和滋养层细胞凋亡增加的结果,也可能是感染所致胎儿宫内发育迟缓、死产、流产等不良妊娠发生的原因。     

孕中期弓形虫感染对BALB/c孕鼠胎盘细胞凋亡的影响

目的探讨孕中期弓形虫感染对BALB/c孕鼠胎盘细胞凋亡的影响.方法在小鼠妊娠第8天采用腹腔注射速殖子法建立弓形虫感染的动物模型,于妊娠第12、14、16、18天分批处死孕鼠,采用流式细胞技术检测胎盘细胞凋亡率,分光光度法测定半胱氨酸天冬氨酸蛋白酶-3(caspase-3)的活性.结果随着妊娠天数的增加,实验组和正常埘照组胎盘细胞凋亡率及caspase-3的活力均在升高,差异均具有统计学意义(P＜0.01);在相同时间,实验组的凋亡率以及酶活力均高于正常对照组,除第18天组胎盘caspase-3活力单位外,其余各组比较差异均具有统计学意义(P＜0.05).结论孕中期弓形虫感染可导致孕鼠胎盘细胞捌亡明显增加.     

重组人IFN-γ对感染弓形虫孕鼠细胞免疫及垂直传播的影响

目的观察重组人IFN-γ对感染弓形虫孕鼠细胞免疫状态及垂直传播的影响。方法取BALB/c孕鼠60只随机分为阳性感染对照组、治疗组及空白对照组。感染对照组与治疗组在孕鼠妊娠第8天用弓形虫速殖子攻击。治疗组于妊娠第7、8、9天用1000UIFN-γ治疗。所有各组孕鼠在妊娠第10、12天尾静脉采抗凝血,流式细胞仪检测CD4^＋、CD8^＋T细胞水平。并在妊娠第12天解剖孕鼠,观察活胎率及胎仔脑组织弓形虫感染情况。结果感染对照组及IFN-γ治疗组与空白对照组比,在孕后第10、12天CD4^＋T细胞水平显著降低,而CD8^＋T细胞水平显著升高,CD4^＋/CD8^＋T细胞比值倒置明显;但治疗组与感染对照组比较,治疗组在妊娠第10、12天CD4^＋T细胞显著升高,CD8^＋T细胞显著降低,CD4^＋/CD8^＋T细胞比值明显升高,活胎率也明显升高,宫内胚胎弓形虫感染率明显降低。结论IFN-γ治疗可以改善感染弓形虫孕鼠的细胞免疫功能,提高孕鼠免疫力,减少垂直传播概率。     

非酶反应对全血谷胱甘肽过氧化物酶活性测定的影响及其消除方法

目的 探讨Hafeman氏改良法测定全血谷胱甘肽过氧化物酶活性时非酶管及抑酶剂的改进。方法 用新选抑酶剂灭活谷胱甘肽过氧化物酶的血稀释液代替蒸馏水做非酶对照管,测定全血谷胱甘肽过氧化物酶活性。结果 用改进后的方法测定谷胱甘肽过氧化物酶活性,较好地剔除了全血的非酶反应,测定结果比Hafeman氏改良法更接近全血的真实水平,回收率为98．7％－100．3％。结论 血中非酶物质远大于蒸馏水中的量,原方法终止酶反应的试剂,不能有效扣除非酶反应,是造成Hafeman氏改良法测定值系统性偏高的主要原因;蒸馏水不能代替血做非酶对照管。     

弓形虫感染妊娠中期BALB/c小鼠对胎鼠生长发育及胎盘系数的影响

目的 探讨弓形虫感染妊娠中期BALB/c小鼠对胎鼠生长发育以及胎盘系数的影响.方法在妊娠第8天采用腹腔注射法建立弓形虫感染的动物模型,于妊娠第12、14、16、18天分批处死孕鼠,分离胎盘胎鼠,解剖显微镜下观察胎鼠存活情况,电子天平称量胎盘和胎鼠重量,游标卡尺测量胎鼠体长和尾长. 结果 随着妊娠天数的增加,实验组孕鼠吸收胎明显增多,出现死胎和流产,正常对照组未见异常;正常对照组胎鼠重量、体长和尾长增加明显(胎鼠重量:40.69±11.63,173.43±30.19,495.56±73.97,967.62±83.34:体长:11.53±0.95,16.83±1.15,20.86±1.25;尾长:5.26±0.56,8.08±0.98,10.54±0.58),胎盘重量呈现先增后减趋势(48.62±11.87,87.14±14.05,94.44±12.29,93.33±13.00),胎盘系数呈降低趋势(1.30±0.52,0.51±0.09,0.20±0.05,0.10±0.02),实验组变化趋势不及正常对照组的明显(胎鼠重量:51.11±13.89,148.16 ±36.09,296.11±58.63;体长:11.51±1.42,14.04±1.59;尾长:4.04±0.95,6.87±0.87;胎盘重量:49.31±9.42,66.41±13.28,52.22±12.15;胎盘系数:1.03±0.32,0.48±0.15,0.18±0.05),组内比较差异均有统计学意义(P<0.05);相同时间点的比较显示除第12天组的胎盘胎鼠重量、第14和16天的胎盘系数,还有第14天的胎鼠体长外,其他数据实验组均低于正常对照组,差异有统计学意义(P<0.05). 结论 弓形虫感染妊娠中期BALB/c小鼠可导致胎盘功能障碍,胎鼠生长发育受限,且随着感染天数的增加,可出现死胎和流产等病理性妊娠.     

锌对缺碘大鼠生长及甲状腺功能的影响

目的观察锌对不同碘营养水平大鼠生长发育及对甲状腺形态和功能的影响。方法应用缺碘饲料喂养Wistar大鼠复制缺碘动物模型，同时设补碘、补复合锌和葡萄糖酸锌、补碘加复合锌组。各组每周称重，实验中测尿碘，3个月时取垂体、甲状腺称重并观察微细结构变化同时测甲状腺激素水平。结果缺碘及补锌组尿碘水平降低；缺碘组体重增加减缓；甲状腺肿大；甲状腺激素T4、FT4降低，T3、FT3升高。补锌组与补碘组体重增加栩一致；补锌组甲状腺重量较缺碘组减轻，甲状腺激素部分恢复。结论缺碘大鼠补锌促进生长发育，降低甲状腺肿大程度，调节甲状腺激素代谢紊乱。     

锌对缺碘受孕大鼠和仔鼠甲状腺功能及脑发育影响的实验研究

目的观察锌对碘缺乏妊娠大鼠及仔鼠生长发育、甲状腺和脑形态与功能及相关激素的影响。方法用低碘饲料喂养Wistar雌性大鼠，同时设补碘、补复合锌、补葡萄糖酸锌、补碘加复合锌组。第90天时将动物模型进行交配，于第21天处死孕鼠，查活胎体质量、畸胎、死胎率和胚胎吸收率，对垂体、甲状腺称质量，测血清甲状腺激素、促性腺激素和性激素水平。各组仔鼠于生后第45天对垂体、甲状腺称质量，测脑组织蛋白质、DNA、RNA水平。结果缺碘组孕鼠尿碘低下，甲状腺肿大，T4、FT4降低（P〈0．01），T3、FT3升高（P〈0．01）；促性腺激素和性激素异常；胎鼠体质量降低，死胎、吸收胎增加；仔鼠体质量增长缓慢，甲状腺肿大，脑质量减轻，蛋白质、DNA、RNA水平减低，同时RNA／DNA和蛋白质／DNA比值降低（P〈0．01）。补锌组孕鼠甲状腺质量较缺碘组减轻（P〈0.01），甲状腺激素、促性腺激素和性激素部分恢复；胎鼠体质量增加，死胎和胚胎吸收率降低；仔鼠甲状腺肿大减轻，体质量增加，脑蛋白质、DNA、RNA水平和RNA／DNA、蛋白质／DNA比值升高（P〈0．01）。结论缺碘大鼠补锌降低甲状腺肿大程度；调节甲状腺激素、促性腺激素和性激素代谢紊乱；其生育的仔鼠甲状腺肿大减轻，大脑蛋白质、DNA、RNA水平增加。由此认为，补锌拮抗由缺碘所致的孕鼠生殖和胎鼠发育异常及仔鼠脑发育障碍。     

锌对缺碘大鼠仔鼠甲状腺和脑发育影响的实验研究

目的 观察不同碘营养水平母鼠生育的仔鼠甲状腺形态、大脑重量及脑组织中蛋白质、DNA、RNA含量变化及锌对其的影响作用。方法 应用缺碘饲料喂养Wistar雌性大鼠复制缺碘动物模型，同时设补碘、补复合锌和葡萄糖酸锌、补碘加复合锌等组。3个月时将动物模型进行交配繁育仔鼠，1个月后处死仔鼠，取垂体、甲状腺进行病理学检查，生物化学方法检测大脑组织中蛋白质、DNA、RNA含量。结果 缺碘组大鼠生育的仔鼠体重增长缓慢，甲状腺肿大，大脑重量减轻，脑中蛋白质、DNA、RNA含量降低，同时RNA／DNA比值和蛋白质／DNA比值降低。补锌组的仔鼠甲状腺肿大程度较缺碘组减轻，体重增加，脑蛋白质、DNA、RNA含量和RNA／DNA、蛋白质／DNA比值升高。结论 原代缺碘大鼠补锌，降低其生育的仔鼠甲状腺肿大程度，使大脑蛋白质、DNA、RNA含量增加，拮抗缺碘所致的脑发育障碍。     

Mild zinc deficiency and dietary phytic acid accelerates the development of fulminant hepatitis in LEC rats

BACKGROUND AND AIM: Restriction of copper intake delays hepatic copper accumulation in Long-Evans Cinnamon (LEC) rats, which are animal models of Wilson's disease. Involvement of zinc is suggested to develop hepatitis in the disease; however, this has not been clarified. The aims of this study were to investigate the effects of mild zinc deficiency on the development of hepatitis and to determine the relationship between the absorption and hepatic levels of copper, zinc and iron. METHODS: Male LEC and F344 (wild type atp7b) rats were fed a low zinc, phytate-containing or control diet. The onset of hepatitis (Experiment 1), and absorptive rates of copper, zinc and iron and hepatitis indices in 4 weeks (Experiment 2) were observed. RESULTS: The onset of fulminant hepatitis in LEC rats was much earlier in the low zinc and phytate groups (mean 94.6 +/- 2.74 days and 82.8 +/- 3.56 days old, respectively) than in the control group (136 +/- 2.11 days old) with worse hepatitis indices. Hepatic copper levels were much higher in LEC rats than F344 rats, but were not largely different among the diet groups without prominent changes in copper absorption. Hepatic levels and intestinal absorption of zinc and iron were lower in the phytate group than in the control group. CONCLUSION: Mild zinc deficiencies caused by a low zinc or phytate-containing diet accelerate the onset of hepatitis in LEC rats without increasing copper absorption, and zinc and iron metabolism may be involved in the earlier onset of jaundice of LEC rats.     

Hepatocyte growth factor,epidermal growth factor,and placenta growth factor concentrations in peripheral blood of pregnant women with alcohol abuse

BACKGROUND: Alcohol abuse during pregnancy compromises fetal development not only directly but also by abnormal placental function. Therefore, hepatocyte growth factor (HGF), epidermal growth factor (EGF), and placenta growth factor (PlGF), expressed in the placenta, may play a role in alcohol-induced placental dysfunction. METHODS: Peripheral venous blood samples were collected from 40 pregnant alcohol-abusing women and 42 abstinent pregnant women from gestational weeks 4 to 41. Plasma HGF and serum PlGF were assessed by enzyme-linked immunosorbent assays and serum EGF by an immunofluorometric assay. RESULTS: Plasma HGF concentrations were similar in alcohol-abusing and abstinent mothers, although in the latter women these concentrations increased with advancing pregnancy. Serum EGF concentrations were consistently higher in alcohol-abusing than in abstinent mothers. In the latter, these concentrations decreased with advancing pregnancy. Serum PlGF concentrations increased with advancing pregnancy in both groups and were higher in alcohol-abusing mothers during the second and third trimesters but not during the first. CONCLUSIONS: Alcohol abuse during pregnancy is associated with changes in maternal circulating EGF and PlGF but not HGF concentrations. The observed changes may be caused by alcohol per se or may be secondary to possible alcohol-induced changes in placental physiology.     

Growth hormone levels in the diagnosis of growth hormone deficiency in adulthood

Current guidelines for the diagnosis of adult growth hormone deficiency (GHD) state that the diagnosis must be proven biochemically by provocative testing that is done within the appropriate clinical context. The need for reliance on provocative testing is based on evidence that the evaluation of spontaneous growth hormone (GH) secretion over 24 h and the measurement of IGF-I and IGFBP-3 levels do not distinguish between normal and GHD subjects. Regarding IGF-I, it has been demonstrated that very low levels in patients highly suspected for GHD (i.e., patients with childhood-onset, severe GHD, or with multiple hypopituitarism acquired in adulthood) may be considered definitive evidence for severe GHD obviating the need for provocative tests. However, normal IGF-I levels do not rule out severe GHD and therefore adults suspected for GHD and with normal IGF-I levels must undergo a provocative test of GH secretion. The insulin tolerance test (ITT) is the test of choice, with severe GHD being defined by a GH peak less than 3 microg/l, the cut-off that distinguishes normal from GHD adults. The ITT is contraindicated in the presence of ischemic heart disease, seizure disorders, and in the elderly. Other tests are as reliable as the ITT, provided they are used with appropriate cut-off limits. Glucagon stimulation, a classical test, and especially new maximal tests such as GHRH in combination with arginine or GHS (i.e., GHRP-6) have well-defined cut-off limits, are reproducible, are independent of age and gender, and are able to distinguish between normal and GHD subjects. The confounding effect of overweight or obesity on the interpretation of the GH response to provocative tests needs to be considered as the somatotropic response to all stimuli is negatively correlated with body mass index. Appropriate cut-offs for lean, overweight, and obese subjects must be used in order to avoid false-positive diagnoses of severe GHD in obese adults.     

碘铁联合缺乏对大鼠血脂水平的影响

目的 通过控制碘、铁摄入量,造成缺铁、缺碘模型,研究碘、铁缺乏对大鼠血脂水平的影响.方法 将Sprauge-Dawley (SD)雄性大鼠随机分为4组:正常对照组(N组,饲料碘含量362.0 μg/kg,铁含量93.3 mg/kg),碘缺乏组(ID组,饲料碘含量61.4 μg/kg,铁含量93.3 mg/kg),铁缺乏...     

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成人生长激素缺乏症(GHD)最常见于下丘脑和(或)垂体结构破坏或功能损害,临床上主要根据一系列非特异性临床表现及相应的生化指标来确诊。由于生长激素(GH)的脉冲式分泌及正常人群随机GH测定值的波动,GHD患者不能仅依据随机GH结果与正常人群相鉴别。目前国际上公认的成人GHD诊断金标准是胰岛素低血糖试验(ITT),近年来认为生长激素释放激素(GHRH)+精氨酸试验,GH-RH+生长激素释放肽(GHRP)及胰高血糖素兴奋试验的诊断价值与ITT相当。成人GHD常合并多种并发症,其中慢性心血管系统并发症可能是导致该类患者病死率增加的主要原因。而重组人生长激素(rh-GH)替代治疗可以改善这部分患者的许多临床终点事件,包括生活质量的提高及心血管风险的降低等。     

衰老和缺锌大鼠海马生长抑素含量及其阳性神经元的变化

目的 探讨海马结构内生长抑素（ＳＳ）含量及其阳性神经元的增龄变化，并分析这种变化与衰老过程中锌水平的降低的关系。方法 选用Ｗｉｓｔａｒ雄性大鼠４２只，分为锌组（７月龄）、老年组（２４月龄）和对照组（７月龄），每组各１４只。老年组和对照组均普食喂养，缺锌组以含１００ｍｇ／ｋｇ双硫腙的普食喂养。２周后，采用放免分析和原子吸收法，测定每组各８史大鼠海马和血浆ＳＳ含量及血浆锌含量；采用免疫组化ＡＢＣ法结合