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2
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本文引用的文献

1
Coding nucleotide sequence of 3-methylcholanthrene-inducible cytochrome P-450d cDNA from rat liver.大鼠肝脏中3-甲基胆蒽诱导型细胞色素P-450d cDNA的编码核苷酸序列。
Proc Natl Acad Sci U S A. 1984 Mar;81(6):1649-53. doi: 10.1073/pnas.81.6.1649.
2
The murine Ah locus. Comparison of the complete cytochrome P1-450 and P3-450 cDNA nucleotide and amino acid sequences.小鼠Ah基因座。细胞色素P1 - 450和P3 - 450完整cDNA核苷酸及氨基酸序列的比较。
J Biol Chem. 1984 Sep 10;259(17):10705-13.
3
Titration of mRNAs for cytochrome P-450c and P-450d under drug-inductive conditions in rat livers by their specific probes of cloned DNAs.在药物诱导条件下，利用克隆DNA的特异性探针滴定大鼠肝脏中细胞色素P - 450c和P - 450d的mRNA。
J Biol Chem. 1984 Aug 25;259(16):10145-9.
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Effect of ethanol on nitrosamine metabolism and distribution. Implications for the role of nitrosamines in human cancer and for the influence of alcohol consumption on cancer incidence.
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Aryl hydrocarbon hydroxylase induction levels in patients with malignant tumors associated with smoking.与吸烟相关的恶性肿瘤患者中芳烃羟化酶的诱导水平。
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Metabolic oxidation phenotypes as markers for susceptibility to lung cancer.代谢氧化表型作为肺癌易感性的标志物。
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Purification of liver microsomal cytochrome P-450 isozymes 3a and 6 from imidazole-treated rabbits. Evidence for the identity of isozyme 3a with the form obtained by ethanol treatment.
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Purification and characterization of six cytochrome P-450 isozymes from human liver microsomes.从人肝微粒体中纯化和鉴定六种细胞色素P-450同工酶。
Biochemistry. 1983 Nov 8;22(23):5375-83. doi: 10.1021/bi00292a019.
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Nucleotide sequence of a full-length cDNA coding for 3-methylcholanthrene-induced rat liver cytochrome P-450MC.编码3-甲基胆蒽诱导的大鼠肝脏细胞色素P-450MC的全长cDNA的核苷酸序列。
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10
Positive correlation between high aryl hydrocarbon hydroxylase activity and primary lung cancer as analyzed in cryopreserved lymphocytes.在冷冻保存的淋巴细胞中分析发现，高芳烃羟化酶活性与原发性肺癌之间存在正相关。
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细胞色素P450与人类癌症

P450 and human cancer.

作者信息

Kawajiri K, Fujii-Kuriyama Y

机构信息

Department of Biochemistry, Saitama Cancer Center Research Institute.

出版信息

Jpn J Cancer Res. 1991 Dec;82(12):1325-35. doi: 10.1111/j.1349-7006.1991.tb01800.x.

DOI:10.1111/j.1349-7006.1991.tb01800.x
PMID:1778754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5918357/
Abstract

Most of the chemical carcinogens in our environment are activated mainly by a restricted number of cytochrome P450 species, P450 1A1, 1A2, 2E1, and 3A. This metabolic activation of procarcinogens is a crucial part of the initial host response to the environmental exposure, since most chemical carcinogens do not show any carcinogenicity by themselves. Inter-individual variability in the metabolic activity may thus be a key host factor to explain the differences in susceptibility to chemical carcinogenesis among individuals. Recent studies on P450s in cancer etiology have provided some valuable insights into this problem.

摘要

我们环境中的大多数化学致癌物主要由数量有限的细胞色素P450同工酶激活，即P450 1A1、1A2、2E1和3A。前致癌物的这种代谢激活是宿主对环境暴露初始反应的关键部分，因为大多数化学致癌物本身并不显示任何致癌性。代谢活性的个体间差异因此可能是解释个体对化学致癌易感性差异的关键宿主因素。最近关于细胞色素P450在癌症病因学方面的研究为这个问题提供了一些有价值的见解。