Singal P K, MacLeod B, Deally C M
Cardiovascular Sciences Division, St. Boniface General Hospital Research Centre, Winnipeg, Canada.
Mol Cell Biochem. 1988 May;81(1):89-94. doi: 10.1007/BF00225656.
Chronic treatment of rats with adriamycin has been shown to affect myocardial lysosomes as well as enzyme activities in the serum fraction. In this study, we examined in vitro effects of adriamycin (10(-6) to 10(-3) M) on the lysosomal fraction isolated from rat ventricular tissue. Morphological examination revealed that the isolated fraction was mainly vesicular in nature. Higher concentrations of adriamycin (10(-3) M) caused a significant loss of acid phosphatase and N-acetyl-B-D-glucosaminidase activity from the lysosomal vesicles. The enzyme leakage was not accompanied by any intravesicular localization of lanthanum, an extravesicular electron dense tracer. Preincubation of lysosomal vesicles with 10 micrograms/ml superoxide dismutase did not protect against adriamycin-induced loss of lysosomal enzymes. The study shows that adriamycin induces loss of lysosomal enzymes in vitro and the superoxide radical may not be involved in this change.
已证明用阿霉素长期治疗大鼠会影响心肌溶酶体以及血清部分的酶活性。在本研究中,我们检测了阿霉素(10⁻⁶至10⁻³M)对从大鼠心室组织分离的溶酶体部分的体外作用。形态学检查显示,分离出的部分本质上主要是囊泡状。较高浓度的阿霉素(10⁻³M)导致溶酶体囊泡中酸性磷酸酶和N-乙酰-β-D-葡萄糖苷酶活性显著丧失。酶泄漏并未伴随镧(一种细胞外电子致密示踪剂)在囊泡内的任何定位。用10微克/毫升超氧化物歧化酶对溶酶体囊泡进行预孵育并不能防止阿霉素诱导的溶酶体酶丧失。该研究表明,阿霉素在体外诱导溶酶体酶丧失,超氧自由基可能不参与此变化。