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1.
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.  相似文献   

2.
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.  相似文献   

3.
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.  相似文献   

4.
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.  相似文献   

5.
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.  相似文献   

6.
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.  相似文献   

7.
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.  相似文献   

8.
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.  相似文献   

9.
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.  相似文献   

10.
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.  相似文献   

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