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脂质过氧化和2-烯丙基-2-异丙基乙酰胺导致细胞色素P-450中血红素的丧失。这是一条不涉及一氧化碳产生的异常途径。

Loss of haem from cytochrome P-450 caused by lipid peroxidation and 2-allyl-2-isoprophylacetamide. An abnormal pathway not involving production of carbon monoxide.

作者信息

De Matteis F, Gibbs A H, Unseld A

出版信息

Biochem J. 1977 Dec 15;168(3):417-22. doi: 10.1042/bj1680417.

DOI:10.1042/bj1680417
PMID:606245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1183788/
Abstract
  1. Microsomal preparations undergoing lipid peroxidation produce CO and lose haem from cytochrome P-450. 2. The amount of CO produced does not correlate with the amount of haem lost and, after pre-labelling of microsomal haem in its bridges with 5-amino[5-14C]laevulinate, the radioactivity lost from haem is not recorved as CO. 3. Similarly, when pre-labelled microsomal haem is destroyed by the action of 2-allyl-2-isopropylacetamide, no radioactivity is recovered as CO. In clear contrast, on degradation of haem by the haem oxygenase system, CO is produced in an amount equimolar to the haem lost. 4. It is concluded that (a) the CO produced during lipid peroxidation originates from a source different from haem and (b) the degradations of haem caused by lipid peroxidation and 2-allyl-2-isopropylacetamide do not involve to any significant extent evolution of the methene-bridge carbon of haem as CO.
摘要
  1. 经历脂质过氧化的微粒体制剂会产生一氧化碳,并从细胞色素P-450中失去血红素。2. 产生的一氧化碳量与失去的血红素量不相关,并且在用5-氨基[5-¹⁴C]乙酰丙酸对微粒体血红素的桥进行预标记后,从血红素中损失的放射性不会以一氧化碳的形式回收。3. 同样,当预标记的微粒体血红素被2-烯丙基-2-异丙基乙酰胺作用破坏时,也没有放射性以一氧化碳的形式回收。相比之下,在血红素加氧酶系统降解血红素时,产生的一氧化碳量与失去的血红素量等摩尔。4. 得出的结论是:(a) 脂质过氧化过程中产生的一氧化碳源自与血红素不同的来源;(b) 脂质过氧化和2-烯丙基-2-异丙基乙酰胺引起的血红素降解在很大程度上不涉及血红素的亚甲基桥碳以一氧化碳的形式释放。

相似文献

1
Loss of haem from cytochrome P-450 caused by lipid peroxidation and 2-allyl-2-isoprophylacetamide. An abnormal pathway not involving production of carbon monoxide.脂质过氧化和2-烯丙基-2-异丙基乙酰胺导致细胞色素P-450中血红素的丧失。这是一条不涉及一氧化碳产生的异常途径。
Biochem J. 1977 Dec 15;168(3):417-22. doi: 10.1042/bj1680417.
2
Degradation of cytochrome P-450 haem by carbon tetrachloride and 2-allyl-2-isopropylacetamide in rat liver in vivo and in vitro. Involvement of non-carbon monoxide-forming mechanisms.四氯化碳和2-烯丙基-2-异丙基乙酰胺在大鼠肝脏体内外对细胞色素P-450血红素的降解作用。非一氧化碳生成机制的参与。
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J Clin Invest. 1980 May;65(5):1135-40. doi: 10.1172/JCI109767.
3
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Biochem J. 1981 May 15;196(2):585-9. doi: 10.1042/bj1960585.
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本文引用的文献

1
The formation of carbon monoxide during peroxidation of microsomal lipids.微粒体脂质过氧化过程中一氧化碳的形成。
Biochem Biophys Res Commun. 1976 Dec 20;73(4):850-7. doi: 10.1016/0006-291x(76)90199-6.
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The thiobarbituric acid reagent as a test for the oxidation of unsaturated fatty acids by various agents.硫代巴比妥酸试剂用于检测各种试剂对不饱和脂肪酸的氧化作用。
Arch Biochem. 1949 Dec;24(2):305-13.
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THE CARBON MONOXIDE-BINDING PIGMENT OF LIVER MICROSOMES. I. EVIDENCE FOR ITS HEMOPROTEIN NATURE.肝微粒体的一氧化碳结合色素。I. 其血红蛋白性质的证据。
J Biol Chem. 1964 Jul;239:2370-8.
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CARBON MONOXIDE IN BLOOD: ANALYTICAL METHOD AND SOURCES OF ERROR.血液中的一氧化碳:分析方法与误差来源
J Appl Physiol. 1964 May;19:510-5. doi: 10.1152/jappl.1964.19.3.510.
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A new method of hemin isolation.一种新的氯化血红素分离方法。
Biochim Biophys Acta. 1957 Nov;26(2):437. doi: 10.1016/0006-3002(57)90033-1.
6
Studies on the biosynthesis of blood pigments. I. Haem synthesis in haemolysed erythrocytes of chicken blood.血液色素的生物合成研究。I. 鸡血溶血红细胞中的血红素合成。
Biochem J. 1954 Jan;56(1):156-63. doi: 10.1042/bj0560156.
7
Endogenous production of carbon-14 labeled carbon monoxide: an in vivo technique for the study of heme catabolism.内源性产生的碳-14标记一氧化碳:一种用于研究血红素分解代谢的体内技术。
J Nucl Med. 1966 Sep;7(9):696-707.
8
Reduced triphosphopyridine nucleotide oxidase-catalyzed alterations of membrane phospholipids. IV. Dependence on Fe3+.三磷酸吡啶核苷酸氧化酶催化的膜磷脂变化减少。IV. 对Fe3+的依赖性。
J Biol Chem. 1971 Jan 10;246(1):263-9.
9
A mechanism for the production of ethylene from methional. The generation of the hydroxyl radical by xanthine oxidase.一种由甲硫醛生成乙烯的机制。黄嘌呤氧化酶产生羟基自由基。
J Biol Chem. 1970 Sep 25;245(18):4641-6.
10
Catabolism of heme in vivo: comparison of the simultaneous production of bilirubin and carbon monoxide.体内血红素的分解代谢:胆红素与一氧化碳同时生成的比较。
J Clin Invest. 1970 May;49(5):914-25. doi: 10.1172/JCI106311.