Klebanov G I, POltanov E A, Vladimirov Iu A
Russian State Medical University, ul. Ostrovityanova 1, Moscow, 117997 Russia.
Biofizika. 2003 May-Jun;48(3):462-73.
The effect of lipopolysaccharides (LPS) and low-power laser radiation on nitric oxide (NO) production and the activity of superoxide dismutase (SOD) in rat peritoneal exudate macrophages was investigated. It was found that LPS increased NO production and SOD activity in macrophages in a concentration-dependent manner. The maximal activity of SOD was more than 100 times greater than in the control and was achieved at an LPS concentration of less than 10 ng/ml. The maximal production of NO was more than 250% of the control and was achieved at an LPS concentration of 100 ng/ml. The presence of cycloheximide, a transcriptional synthesis inhibitor, in conditioned media almost completely abolished SOD activation and NO production. This implies that the LPS-induced increase in SOD activity and NO production were determined by the activation of de novo protein synthesis (SOD and inducible NO synthase). The irradiation of macrophages by red light resulted in a dose-dependent increase in NO production and SOD activity. The incubation of irradiated cells in the presence of 10 microM cycloheximide abolished the increase. The presence of antioxidants (mexidol and ascorbate) also significantly inhibited the laser-induced activity of macrophages. Thus, laser irradiation of cells in the red range activates the synthesis of SOD and inducible NO-synthase de novo due to photosensitized initiation of free radical reactions.
研究了脂多糖(LPS)和低功率激光辐射对大鼠腹腔渗出液巨噬细胞中一氧化氮(NO)生成及超氧化物歧化酶(SOD)活性的影响。发现LPS以浓度依赖的方式增加巨噬细胞中NO的生成及SOD的活性。SOD的最大活性比对照组高100倍以上,在LPS浓度低于10 ng/ml时达到。NO的最大生成量是对照组的250%以上,在LPS浓度为100 ng/ml时达到。条件培养基中存在转录合成抑制剂环己酰亚胺几乎完全消除了SOD的激活和NO的生成。这意味着LPS诱导的SOD活性和NO生成的增加是由从头蛋白质合成(SOD和诱导型NO合酶)的激活所决定的。红光照射巨噬细胞导致NO生成和SOD活性呈剂量依赖性增加。在10 microM环己酰亚胺存在下孵育照射后的细胞消除了这种增加。抗氧化剂(美西律和抗坏血酸盐)的存在也显著抑制了激光诱导的巨噬细胞活性。因此,红色波段的激光照射通过自由基反应的光敏引发激活了SOD和诱导型NO合酶的从头合成。