Adriamycin stimulates only the iron ion-induced, NADPH-dependent microsomal alkane formation.
作者信息
Muliawan H, Scheulen M E, Kappus H
出版信息
Biochem Pharmacol. 1982 Oct 1;31(19):3147-50. doi: 10.1016/0006-2952(82)90101-0.
PMID:7150343
Abstract
摘要
相似文献
1
Adriamycin stimulates only the iron ion-induced, NADPH-dependent microsomal alkane formation.阿霉素仅刺激铁离子诱导的、依赖于烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的微粒体烷烃形成。
Biochem Pharmacol. 1982 Oct 1;31(19):3147-50. doi: 10.1016/0006-2952(82)90101-0.
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Adriamycin stimulates NADPH-dependent lipid peroxidation in liver microsomes not only by enhancing the production of O2 and H2O2, but also by potentiating the catalytic activity of ferrous ions.阿霉素不仅通过增强O2和H2O2的生成，还通过增强亚铁离子的催化活性来刺激肝脏微粒体中依赖NADPH的脂质过氧化。
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Stimulation by adriamycin of rat heart and liver microsomal NADPH-dependent lipid peroxidation.阿霉素对大鼠心脏和肝脏微粒体中依赖烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的脂质过氧化作用的刺激。
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Differential effect of silybin on the Fe2+-ADP and t-butyl hydroperoxide-induced microsomal lipid peroxidation.水飞蓟宾对Fe2+-ADP和叔丁基过氧化氢诱导的微粒体脂质过氧化的差异作用。
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Alkane formation during liver microsomal lipid peroxidation.肝脏微粒体脂质过氧化过程中的烷烃形成。
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Enhancement of NADPH-dependent lipid peroxidation activity by ethylene-diamineteraacetic acid (EDTA) in the presence of ferrous ion in rabbit liver microsomes.在兔肝微粒体中，乙二胺四乙酸（EDTA）在亚铁离子存在的情况下增强了NADPH依赖性脂质过氧化活性。
Jpn J Pharmacol. 1977 Oct;27(5):653-7. doi: 10.1254/jjp.27.653.
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Lysis of erythrocytes as a result of microsomal lipid peroxidation induced by CCl4 or FeCl2.由四氯化碳（CCl4）或氯化亚铁（FeCl2）诱导的微粒体脂质过氧化导致的红细胞溶解。
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The effect of the anthrapyrazole antitumour agent CI941 on rat liver microsome and cytochrome P-450 reductase mediated free radical processes. Inhibition of doxorubicin activation in vitro.蒽吡唑类抗肿瘤药物CI941对大鼠肝微粒体及细胞色素P - 450还原酶介导的自由基过程的影响。体外对阿霉素激活的抑制作用。
Biochem Pharmacol. 1987 Oct 15;36(20):3345-51. doi: 10.1016/0006-2952(87)90309-1.
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Further studies on adriamycin induced in vitro lipid peroxidation.阿霉素诱导的体外脂质过氧化的进一步研究。
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Inhibition of hepatic microsomal lipid peroxidation by drug substrates without drug metabolism.药物底物对肝微粒体脂质过氧化的抑制作用，且无药物代谢。
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