Abstract：
BACKGROUND: As an essential trace element, Copper (Cu) participates in numerous physiological and biological reactions in the body. Cu is closely related to heart health, and an imbalance of Cu will cause cardiac dysfunction. The research aims to examine how Cu deficiency affects the heart, assess mitochondrial function in the hearts, and disclose possible mechanisms of its influence.
METHODS: Weaned mice were fed Cu-deficient diets and intraperitoneally given copper sulfate (CuSO4) to correct the Cu deficiency. The pathological change of the heart was assessed using histological inspection. Cardiac function and oxidative stress levels were evaluated by biochemical assay kits. ELISA and ATP detection kits were used to detect the levels of complexes I-IV in the mitochondrial respiratory chain (MRC) and ATP, respectively. Real time PCR was utilized to determine mRNA expressions, and Western blotting was adopted to determine protein expressions, of molecules related to mitochondrial fission and fusion.
RESULTS: Cu deficiency gave rise to elevated heart index, cardiac histological alterations and oxidation injury, increased serum levels of creatine kinase (CK), lactic dehydrogenase (LDH), and creatine kinase isoenzyme MB (CK-MB) together with increased malondialdehyde (MDA) production, decreased the glutathione (GSH), Superoxide Dismutase (SOD), and Catalase (CAT) activities or contents. Besides, Cu deficiency caused mitochondrial damage characterized by decreased contents of complexes I-IV in the MRC and ATP in the heart. In the meantime, Cu deficiency also reduced protein and mRNA expressions of factors associated with mitochondrial fusion, including Mfn1 and Mfn2, while significantly increased factors Drip1 and Fis1 related to mitochondrial fission. However, adding CuSO4 improved the above changes significantly.
CONCLUSIONS: According to research results, Cu deficiency can cause heart damage in mice, along with oxidative damage and mitochondrial dysfunction, which are closely related to mitochondrial fusion and fission disorders.
METHODS: Weaned mice were fed Cu-deficient diets and intraperitoneally given copper sulfate (CuSO4) to correct the Cu deficiency. The pathological change of the heart was assessed using histological inspection. Cardiac function and oxidative stress levels were evaluated by biochemical assay kits. ELISA and ATP detection kits were used to detect the levels of complexes I-IV in the mitochondrial respiratory chain (MRC) and ATP, respectively. Real time PCR was utilized to determine mRNA expressions, and Western blotting was adopted to determine protein expressions, of molecules related to mitochondrial fission and fusion.
RESULTS: Cu deficiency gave rise to elevated heart index, cardiac histological alterations and oxidation injury, increased serum levels of creatine kinase (CK), lactic dehydrogenase (LDH), and creatine kinase isoenzyme MB (CK-MB) together with increased malondialdehyde (MDA) production, decreased the glutathione (GSH), Superoxide Dismutase (SOD), and Catalase (CAT) activities or contents. Besides, Cu deficiency caused mitochondrial damage characterized by decreased contents of complexes I-IV in the MRC and ATP in the heart. In the meantime, Cu deficiency also reduced protein and mRNA expressions of factors associated with mitochondrial fusion, including Mfn1 and Mfn2, while significantly increased factors Drip1 and Fis1 related to mitochondrial fission. However, adding CuSO4 improved the above changes significantly.
CONCLUSIONS: According to research results, Cu deficiency can cause heart damage in mice, along with oxidative damage and mitochondrial dysfunction, which are closely related to mitochondrial fusion and fission disorders.
摘要：
背景：作为必需的微量元素，铜（Cu）参与体内许多生理和生物反应。铜与心脏健康密切相关，铜的失衡会导致心脏功能障碍。这项研究旨在研究铜缺乏如何影响心脏，评估心脏的线粒体功能，并揭示其影响的可能机制。
方法：断奶小鼠饲喂缺铜饮食，腹腔内给予硫酸铜（CuSO4）以纠正缺铜。使用组织学检查评估心脏的病理变化。通过生化测定试剂盒评估心功能和氧化应激水平。ELISA和ATP检测试剂盒检测线粒体呼吸链(MRC)中复合物I-IV和ATP,分别。实时PCR用于确定mRNA表达，采用蛋白质印迹法测定蛋白质表达，与线粒体裂变和融合有关的分子。
结果：铜缺乏导致心脏指数升高，心脏组织学改变和氧化损伤，血清肌酸激酶（CK）水平升高，乳酸脱氢酶（LDH），和肌酸激酶同工酶MB（CK-MB）以及丙二醛（MDA）产生增加，减少谷胱甘肽（GSH），超氧化物歧化酶(SOD),和过氧化氢酶（CAT）活动或内容。此外,铜缺乏导致线粒体损伤，其特征是MRC和心脏ATP中复合物I-IV的含量降低。同时,铜缺乏还降低了与线粒体融合相关的因子的蛋白质和mRNA表达，包括Mfn1和Mfn2，而显着增加了与线粒体裂变相关的因子Drip1和Fis1。然而,CuSO4的加入显著改善了上述变化。
结论：根据研究结果，铜缺乏会导致小鼠心脏损伤，伴随着氧化损伤和线粒体功能障碍，与线粒体融合和裂变障碍密切相关。
方法：断奶小鼠饲喂缺铜饮食，腹腔内给予硫酸铜（CuSO4）以纠正缺铜。使用组织学检查评估心脏的病理变化。通过生化测定试剂盒评估心功能和氧化应激水平。ELISA和ATP检测试剂盒检测线粒体呼吸链(MRC)中复合物I-IV和ATP,分别。实时PCR用于确定mRNA表达，采用蛋白质印迹法测定蛋白质表达，与线粒体裂变和融合有关的分子。
结果：铜缺乏导致心脏指数升高，心脏组织学改变和氧化损伤，血清肌酸激酶（CK）水平升高，乳酸脱氢酶（LDH），和肌酸激酶同工酶MB（CK-MB）以及丙二醛（MDA）产生增加，减少谷胱甘肽（GSH），超氧化物歧化酶(SOD),和过氧化氢酶（CAT）活动或内容。此外,铜缺乏导致线粒体损伤，其特征是MRC和心脏ATP中复合物I-IV的含量降低。同时,铜缺乏还降低了与线粒体融合相关的因子的蛋白质和mRNA表达，包括Mfn1和Mfn2，而显着增加了与线粒体裂变相关的因子Drip1和Fis1。然而,CuSO4的加入显著改善了上述变化。
结论：根据研究结果，铜缺乏会导致小鼠心脏损伤，伴随着氧化损伤和线粒体功能障碍，与线粒体融合和裂变障碍密切相关。
