Rakotovao Andry, Tanguy Stéphane, Toufektsian Marie-Claire, Berthonneche Corinne, Ducros Véronique, Tosaki Arpad, de Leiris Joël, Boucher François
Laboratoire NVMC-EA 3746, IFRT 130 Ingénierie pour le Vivant, Bâtiment Jean Roget-Domaine de la Merci, Université Joseph Fourier, 38700 La Tronche, France.
J Trace Elem Med Biol. 2005;19(1):43-7. doi: 10.1016/j.jtemb.2005.07.001.
Recent studies have demonstrated that electrical uncoupling at gap junctions during ischemia is associated with cardiac Connexin-43 (Cx43) dephosphorylation. Whether oxidative stress is involved in this phenomenon still remains unclear. In the present study, we examined the influence of selenium intake on reperfusion-induced Cx43 dephosphorylation. Male Wistar rats were fed a diet containing either 0.05 mg/kg (Low-Se, n = 13) or 1.5 mg/kg (High-Se, n = 11) selenium for 8 weeks. At the end of this diet, hearts were isolated and subjected to 10 min regional ischemia followed by 10 min reperfusion. The level of dephosphorylated Cx43 was determined in tissue samples from ischemic/reperfused and non-ischemic regions of the hearts. At the end of the experiemental diet, the activity of the antioxidant enzyme glutathione peroxidase (GSH-Px) was increased in high-Se hearts compared with low-Se hearts (+ 13%; p < 0.05). After ischemia/reperfusion, in low-Se hearts, Cx43 dephosphorylation appeared significantly increased in the left ventricle compared to the non-ischemic right ventricle (+ 149%; p < 0.05). The high-Se diet significantly reduced Cx43 dephosphorylation in the left ventricle (p < 0.05 vs. low-Se diet). In conclusion, our results suggest that oxidative stress may be involved in Cx43 dephosphorylation during myocardial ischemia/reperfusion, thereby contributing to arrhythmogenesis.
近期研究表明，缺血期间间隙连接的电去偶联与心脏连接蛋白43（Cx43）的去磷酸化有关。氧化应激是否参与此现象仍不清楚。在本研究中，我们检测了硒摄入对再灌注诱导的Cx43去磷酸化的影响。雄性Wistar大鼠喂食含0.05 mg/kg（低硒组，n = 13）或1.5 mg/kg（高硒组，n = 11）硒的饮食8周。在该饮食结束时，分离心脏并进行10分钟局部缺血，随后再灌注10分钟。测定心脏缺血/再灌注和非缺血区域组织样本中去磷酸化Cx43的水平。在实验饮食结束时，高硒组心脏中抗氧化酶谷胱甘肽过氧化物酶（GSH-Px）的活性比低硒组心脏增加（+ 13%；p < 0.05）。缺血/再灌注后，与非缺血的右心室相比，低硒组心脏左心室中Cx43去磷酸化明显增加（+ 149%；p < 0.05）。高硒饮食显著降低了左心室中Cx43的去磷酸化（与低硒饮食相比，p < 0.05）。总之，我们的结果表明氧化应激可能参与心肌缺血/再灌注期间的Cx43去磷酸化，从而导致心律失常的发生。
