Díaz-Elizondo Jessica, Chiong Mario, Rojas-Rivera Diego, Olea-Azar Claudio, Kwon H Moo, Lavandero Sergio
Departamento Bioquímica y Biología Molecular, Universidad de Chile, Santiago 8380492, Chile.
Biochem Biophys Res Commun. 2006 Dec 1;350(4):1076-81. doi: 10.1016/j.bbrc.2006.10.004. Epub 2006 Oct 9.
Cells have developed compensatory mechanisms to restore cell volume, and the ability to resist osmotic swelling or shrinkage parallels their resistance to necrosis or apoptosis. There are several mechanisms by which cells adapt to hyposmotic stress including that of regulatory volume decrease. In ischemia and reperfusion, cardiomyocytes are exposed to hyposmotic stress, but little is known as to how their volume is controlled. Exposure of cultured neonatal rat cardiomyocytes to hyposmotic media induced a rapid swelling without any compensatory regulatory volume decrease. The hyposmotic stress increased the production of reactive oxygen species, mainly through NADPH oxidase. Adenoviral overexpression of catalase inhibited the hyposmosis-dependent OH(*) production, induced the regulatory volume decrease mechanism, and prevented cell death. These results suggest that hyposmotic stress of cardiomyocytes stimulates production of reactive oxygen species which are closely linked to volume regulation and cell death.
细胞已发展出恢复细胞体积的代偿机制，抵抗渗透性肿胀或收缩的能力与它们对坏死或凋亡的抵抗能力相当。细胞适应低渗应激有多种机制，包括调节性容积减小机制。在缺血和再灌注过程中，心肌细胞会受到低渗应激，但关于其体积如何被控制却知之甚少。将培养的新生大鼠心肌细胞暴露于低渗培养基中会导致快速肿胀，且没有任何代偿性调节性容积减小。低渗应激主要通过NADPH氧化酶增加活性氧的产生。过氧化氢酶的腺病毒过表达抑制了低渗依赖性OH(*)的产生，诱导了调节性容积减小机制，并防止了细胞死亡。这些结果表明，心肌细胞的低渗应激刺激了与容积调节和细胞死亡密切相关的活性氧的产生。
