Ghosh S K, Roychoudhury S, Kar S, Ghosh J J, Chakraborti T, Chakraborti S
Department of Biochemistry and Biophysics, University of Kalyani, India.
Indian J Biochem Biophys. 1996 Feb;33(1):57-61.
The role of hydroxyl radical (OH.) in H2O2-mediated stimulation of lipid peroxidation in microsomes of bovine pulmonary arterial smooth muscle tissue and the protective effects of DIDS, the anion channel blocker have been studied. Treatment of microsomes with H2O2 (1 mM) stimulate iron release, OH. production and lipid peroxidation. Pretreatment with DFO (an iron chelator) or DMTU (a hydroxyl radical scavenger) prevents OH. production and thereby reduces lipid peroxidation without any appreciable reduction of iron release. Simultaneous treatment of either DFO or DMTU with H2O2 significantly reduces lipid peroxidation and prevents OH. production without any significant reduction of iron release. However, addition of DFO or DMTU 2 min after treatment of the microsome with H2O2 does not produce any significant reduction of lipid peroxidation, OH production and iron release. Pretreatment of microsomes with DIDS markedly reduces the stimulation of lipid peroxidation without appreciably altering the increase in OH. production and iron release caused by H2O2.
研究了羟自由基（OH.）在H2O2介导的牛肺动脉平滑肌组织微粒体脂质过氧化刺激中的作用以及阴离子通道阻滞剂DIDS的保护作用。用H2O2（1 mM）处理微粒体可刺激铁释放、OH.生成和脂质过氧化。用DFO（一种铁螯合剂）或DMTU（一种羟自由基清除剂）预处理可防止OH.生成，从而减少脂质过氧化，而铁释放没有明显减少。DFO或DMTU与H2O2同时处理可显著降低脂质过氧化并防止OH.生成，而铁释放没有显著减少。然而，在用H2O2处理微粒体2分钟后添加DFO或DMTU，脂质过氧化、OH生成和铁释放没有显著减少。用DIDS预处理微粒体可显著降低脂质过氧化刺激，而不会明显改变H2O2引起的OH.生成和铁释放增加。
