Gurkalo V K
Tsitologiia. 1979 Nov;21(11):1363-7.
The induced chemoluminescence in rat liver mitochondrial preparations was studied in the course of 2-acetylaminofluorene or N-nitrozodiethylamine induced hepatocarcinogenesis. As follows from the literature, the intensity of chemoluminescence is representative of catalase activity, i. e. of one of mitochondrial enzymes. Beginning from the stage of stimulation of pretumor cell proliferation, the course of carcinogenesis is caracterized by a progressive decrease in the intensity of chemoluminescence. An adrenomimetic noradrenaline induced a similar effect, whereas isoprenaline and alpha-adrenoblocator pirroxane stimulated chemoluminescence of mitochondria preparation in the intact rats. Ortobenzoquinone being oxidated with H2O2, noradrenaline and isoproteranol were deprived of oxidative activity. It is suggested that inhibition of mitochondrial catalase activity with endogeneous noradrenaline constitues a primary mechanism of the decrease in chemoluminescence intensity.
在2-乙酰氨基芴或N-亚硝基二乙胺诱导的肝癌发生过程中,对大鼠肝脏线粒体提取物中的诱导化学发光进行了研究。从文献可知,化学发光强度代表过氧化氢酶活性,即线粒体酶之一的活性。从癌前细胞增殖受刺激阶段开始,癌症发生过程的特征是化学发光强度逐渐降低。一种拟肾上腺素去甲肾上腺素可诱导类似效应,而异丙肾上腺素和α-肾上腺素阻断剂哌罗克生则刺激完整大鼠线粒体提取物的化学发光。邻苯醌被过氧化氢氧化后,去甲肾上腺素和异丙肾上腺素失去氧化活性。提示内源性去甲肾上腺素对线粒体过氧化氢酶活性的抑制是化学发光强度降低的主要机制。