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在雌性大鼠心脏线粒体中,卵巢切除导致氧化磷酸化作用丧失。

In female rat heart mitochondria, oophorectomy results in loss of oxidative phosphorylation.

作者信息

Pavón Natalia, Cabrera-Orefice Alfredo, Gallardo-Pérez Juan Carlos, Uribe-Alvarez Cristina, Rivero-Segura Nadia A, Vazquez-Martínez Edgar Ricardo, Cerbón Marco, Martínez-Abundis Eduardo, Torres-Narvaez Juan Carlos, Martínez-Memije Raúl, Roldán-Gómez Francisco-Javier, Uribe-Carvajal Salvador

机构信息

Departamento de FarmacologíaInstituto Nacional de Cardiología Ignacio Chávez, México, Mexico

Departamento de Genética MolecularInstituto de Fisiología Celular, Universidad Nacional Autónoma de México, México D.F., Mexico.

出版信息

J Endocrinol. 2017 Feb;232(2):221-235. doi: 10.1530/JOE-16-0161. Epub 2016 Nov 21.

DOI:10.1530/JOE-16-0161
PMID:27872198
Abstract

Oophorectomy in adult rats affected cardiac mitochondrial function. Progression of mitochondrial alterations was assessed at one, two and three months after surgery: at one month, very slight changes were observed, which increased at two and three months. Gradual effects included decrease in the rates of oxygen consumption and in respiratory uncoupling in the presence of complex I substrates, as well as compromised Ca buffering ability. Malondialdehyde concentration increased, whereas the ROS-detoxifying enzyme Mn superoxide dismutase (MnSOD) and aconitase lost activity. In the mitochondrial respiratory chain, the concentration and activity of complex I and complex IV decreased. Among other mitochondrial enzymes and transporters, adenine nucleotide carrier and glutaminase decreased. 2-Oxoglutarate dehydrogenase and pyruvate dehydrogenase also decreased. Data strongly suggest that in the female rat heart, estrogen depletion leads to progressive, severe mitochondrial dysfunction.

摘要

成年大鼠卵巢切除影响心脏线粒体功能。在手术后1个月、2个月和3个月评估线粒体改变的进展情况:1个月时观察到非常轻微的变化,这些变化在2个月和3个月时增加。逐渐出现的影响包括在存在复合体I底物时氧消耗率和呼吸解偶联的降低,以及钙缓冲能力受损。丙二醛浓度增加,而ROS解毒酶锰超氧化物歧化酶(MnSOD)和乌头酸酶失去活性。在线粒体呼吸链中,复合体I和复合体IV的浓度和活性降低。在其他线粒体酶和转运蛋白中,腺嘌呤核苷酸载体和谷氨酰胺酶减少。2-氧代戊二酸脱氢酶和丙酮酸脱氢酶也减少。数据强烈表明,在雌性大鼠心脏中,雌激素耗竭导致进行性、严重的线粒体功能障碍。

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