Miyahara M, Watanabe Y, Edashige K, Yagyu K
Department of Medical Biology, Kochi Medical School, Japan.
Biochim Biophys Acta. 1993 May 8;1177(1):61-70. doi: 10.1016/0167-4889(93)90158-l.
Without the addition of any exogenous stimuli, neutrophils generated O2- and then ceased in a reversible manner that correlated with cellular swelling and contraction. The nature of the possible mechanism responsible for this O2- generation was studied and compared with that observed in the triggering of stimulant-dependent O2- generation (respiratory burst). The swelling-induced O2- generation was inhibited by diphenyliodonium, and was independent of the functional distortion of mitochondrial and/or microsomal electron transport and xanthine oxidase. This suggested that such generation was involved in respiratory-burst oxidase activation; however, this generation was not accompanied by any new phosphorylation of the 47-kDa protein or of tyrosine proteins. Dihydrocytochalasin B potentiated the O2- generation. The cellular swelling produced a priming effect on the triggering of respiratory burst with different stimuli. Cellular contraction, conversely, suppressed the respiratory burst. The structural specificity of the swelling-induced plasma membrane modulation for the O2- generation was suggested by the finding that modulation of plasma membrane structures by various non-ionic detergents per se inhibited O2- generation. Lipophilic and positively-charged agents inhibited the generation and this inhibition was abrogated by negatively-charged, but not by non-ionic agents. Negatively-charged agents potentiated the O2- generation. These results suggest that both the interaction of the plasma membrane with the cytoskeleton and an increase in net negative charges at the plasma membrane play important role in evoking O2- generation; this is discussed and compared with the signal transduction reported previously for respiratory burst.
在不添加任何外源性刺激的情况下，中性粒细胞产生超氧阴离子（O₂⁻），然后以与细胞肿胀和收缩相关的可逆方式停止。研究了负责这种O₂⁻产生的可能机制的性质，并将其与在刺激依赖性O₂⁻产生（呼吸爆发）触发中观察到的机制进行了比较。肿胀诱导的O₂⁻产生受到二苯基碘鎓的抑制，并且独立于线粒体和/或微粒体电子传递以及黄嘌呤氧化酶的功能畸变。这表明这种产生与呼吸爆发氧化酶的激活有关；然而，这种产生并没有伴随着47 kDa蛋白或酪氨酸蛋白的任何新的磷酸化。双氢细胞松弛素B增强了O₂⁻的产生。细胞肿胀对不同刺激引发的呼吸爆发产生了启动作用。相反，细胞收缩抑制了呼吸爆发。各种非离子洗涤剂本身对质膜结构的调节抑制了O₂⁻的产生，这一发现表明了肿胀诱导的质膜调节对O₂⁻产生的结构特异性。亲脂性和带正电荷的试剂抑制了这种产生，而带负电荷的试剂（而非非离子试剂）可消除这种抑制。带负电荷的试剂增强了O₂⁻的产生。这些结果表明，质膜与细胞骨架的相互作用以及质膜净负电荷的增加在引发O₂⁻产生中起重要作用；对此进行了讨论，并与先前报道的呼吸爆发信号转导进行了比较。
