硒、蛋白质和维生素E联合缺乏致大鼠甲状腺损伤的实验研究

目的 探讨长期低硒、低蛋白质和低维生素E(VE)膳食对大鼠甲状腺组织及其激素代谢的影响.方法 Wistar大鼠40只,按体质量随机分为4组:低硒低蛋白低VE组、低硒低蛋白常VE组、常硒常蛋白低VE组、常硒常蛋白常VE组.饲养至第26周处死,测定大鼠全血谷胱甘肽过氧化物酶(GSH-Px)和肝脏Ⅰ型5'-脱碘酶(ID Ⅰ)活性,血清活性氧(ROS)、丙二醛(MDA)、三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)和促甲状腺激素(TSH)水平;光镜下观察甲状腺组织病理学改变.结果 ①硒+蛋白质和vE对大鼠全血GSH-Px和肝脏ID Ⅰ活性的影响均无交互作用(F值分别为0.003、0.871,P＞0.05),但对血清MDA和ROS水平的影响均存在交互作用(F值分别为13.057、6.706,P＜0.05或＜0.01).②硒+蛋白质和VE对血清T3、T4水平均有影响(F值分别为431.977、28.271、6.570、41.419,P＜0.05).但均无交互作用(F值分别为0.871、0.136,P＞0.05).无论在低硒低蛋白还是常硒常蛋白条件下,常VE组T4水平[(79.095±12.199)、(64.392±6.261)μg/L]均高于低VE组[(61.068±6.648)、(44.176±7.090)μg/L],差异有统计学意义(t值分别为3.670、6.045,P＜0.01);在低VE条件下,常硒常蛋白组T3、T4水平[(0.718±0.079)、(44.176±7.090)μg/L]均低于低硒低蛋白组[(0.966±0.156)、(61.068±6.648)μg/L],差异有统计学意义(t值分别为4.568、4.916,P＜0.01);在常VE条件下,常硒常蛋白组Td水平[(64.392±6.261)μg/L]低于低硒低蛋白组[(79.095±12.199)μg/L],差异有统计学意义(t=3.033,P＜0.01).③低硒低蛋白低VE膳食大鼠甲状腺滤泡上皮细胞出现变性坏死,而补充VE可减轻这种损伤:常硒常蛋白低VE膳食大鼠偶见滤泡腔内胶质稀疏.结论 长期低硒、低蛋白、低VE膳食可导致大鼠体内含硒酶活性降低,从而引起机体氧化代谢产物堆积,甲状腺组织出现病理性损伤,其激素代谢紊乱,而在低硒、低蛋白膳食中补充适量VE可部分降低这种损伤现象.     

硒和蛋白质与大鼠心肌GPX1、GPX4表达及翻译

目的研究硒和蛋白质对大鼠心肌GPX1、GPX4表达及其翻译过程的影响。方法 60只雄性Wistar大鼠按硒与蛋白质两因素两水平的析因设计随机分为四组,饲养一年后处死,western blot方法检测心肌GPX1、GPX4和SBP2蛋白表达水平;RT-PCR方法扩增心肌GPX1、GPX4 mRNA上SECIS序列,SSCP法确定其基因型后进行碱基序列测定。结果低硒组心肌组织GPX1、GPX4含量低于常硒组（P〈0.001;P〈0.05）,SBP2含量高于常硒组（P〈0.05）;低蛋白组心肌组织GPX1含量低于常蛋白组（P〈0.001）,SBP2含量高于常蛋白组（P〈0.05）;硒与蛋白质在影响心肌GPX1表达方面有交互作用（P〈0.001）;GPX1、GPX4基因的SECIS碱基序列并未发生变异。结论在低硒低蛋白条件下,心肌GPX1和GPX4含量显著降低,而SBP2含量则增加;GPX1、GPX4基因的SECIS碱基序列并未发生变异。     

硒和蛋白质对大鼠心肌蛋白质及DNA修复酶的影响

目的 研究低硒低蛋白引起的氧化应激对大鼠心肌蛋白质及DNA修复酶的影响.方法 60只健康雄性Wistar大鼠,按体重随机分为4组,每组15只:低硒低蛋白组(A)、常硒低蛋白组(B)、低硒常蛋白组(C)和常硒常蛋白组(D),饲养1年.处死后,采用2,4-二硝基苯肼(DNPH)比色法检测大鼠心肌蛋白质羰基的含量;提取心肌组...     

克山病患者抗氧化能力测定

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group [(34.80±13.30) μg/L], GSH-Px[(104.10±34.19)U/L]and T-SOD[(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group [(41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group [(48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group[(7.12± 1.37)μmol/L]was higher than that in the internal control group[(5.36±1.18)μmol/L]and the external control group[(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.     

克山病患者抗氧化能力测定

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group [(34.80±13.30) μg/L], GSH-Px[(104.10±34.19)U/L]and T-SOD[(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group [(41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group [(48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group[(7.12± 1.37)μmol/L]was higher than that in the internal control group[(5.36±1.18)μmol/L]and the external control group[(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.     

克山病发病危险因素的病例对照研究

目的探讨克山病发病的危险因素，为制定克山病防治措施提供依据。方法在黑龙江省克山病病区选取41例克山病患者作为病例组．另选134例健康人作为对照组，采用氢化物发生原子荧光光度法检测病例组和对照组全血含硒量．采用5，5’-二硫双-2-硝基苯甲酸（DTNB）分光光度法检测全血谷胱苷肽过氧化物酶（GSH—Px）活力：同时对病例组和对照组进行克山病危险因素的问卷调查，先用单因素卡方检验筛选有意义变量，再引入多因素Logistic回归模型进行综合分析。结果全血含硒量病例组[（34．86±13.14）μg／L]明显低于时照组[（40．97±13．62）μg／L]，两组比较差异有统计学意义（t=2．254，P〈0．05）；GSH—Px活力病例组[（104．10±34．19）U／L]明显低于对照组[（118．57±25．49）U／L]．两组比较差异有统计学意义（t=2．312，P〈0.05）。在问卷调查中，经卡方检验和多因素Logistic回归分析，发现年人均收入水平[比值比（OR）=2.570]、肉类（OR=0．284）和蛋类（OR=0．347）的摄入次数与克山病发生有统计学联系，结论在克山病病区人群中，机体内全血含硒量和GSH—Px活力的下降、年人均收入水平低很可能是克山病发病的危险因素，动物性蛋白摄入的增加可能对克山病的发病起到保护作用：     

克山病患者抗氧化能力测定

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group [(34.80±13.30) μg/L], GSH-Px[(104.10±34.19)U/L]and T-SOD[(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group [(41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group [(48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group[(7.12± 1.37)μmol/L]was higher than that in the internal control group[(5.36±1.18)μmol/L]and the external control group[(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.     

硒和维生素E对大鼠的抗氧化作用

目的研究硒和维生素E(VE)在抗氧化损伤过程中的单独及联合作用。方法80只健康雄性Wistar大鼠,按体质量随机分为4组(每组20只):低硒低VE组、低硒补VE组、补硒低VE组、补硒补VE组。饲养3个月后,乙醚麻醉活杀,采腹主动脉血,离心制备血浆,测定各组大鼠谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)、活性氧(ROS)和丙二醛(MDA)水平。结果①与低硒组比较(不考虑VE),补硒组SOD、GSH-Px、T-AOC活性高于低硒组,而补硒组MDA、ROS水平低于低硒组,差异均有统计学意义(P<0.01);与低VE组比较(不考虑硒),补VE组SOD、T-AOC活性高于低VE组,而GSH-Px、MDA水平低于低VE组,差异均有统计学意义(P<0.05)。②在对SOD、GSH-Px、T-AOC活性及MDA、ROS水平影响方面,硒和VE的主效应分别为:23.05、6.75 kU/L;350.21、-20.73μmol/L;1.99、1.67 kU/L;-0.89、-0.78μmol/L;-199.71、-17.43 kU/L。③硒与VE的协同作用在提高SOD、GSH-Px活性方面比较明显(P<0.05)。结论补充硒和VE能够增强机体抗氧化能力,防止脂质过氧化损伤。但二者的作用强度不同,在补硒0.25 mg/L和补VE 0.2/kg条件下,硒的抗氧化作用明显高于VE,并且硒和VE在提高抗氧化能力方面有明显协同作用。     

克山病患者抗氧化能力测定

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group [(34.80±13.30) μg/L], GSH-Px[(104.10±34.19)U/L]and T-SOD[(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group [(41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group [(48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group[(7.12± 1.37)μmol/L]was higher than that in the internal control group[(5.36±1.18)μmol/L]and the external control group[(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.     

克山病患者抗氧化能力测定

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group [(34.80±13.30) μg/L], GSH-Px[(104.10±34.19)U/L]and T-SOD[(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group [(41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group [(48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group[(7.12± 1.37)μmol/L]was higher than that in the internal control group[(5.36±1.18)μmol/L]and the external control group[(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.