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过氧化应激和年龄对大鼠DNA中脱氧鸟苷-丙二醛加合物浓度的影响。

Effects of peroxidative stress and age on the concentration of a deoxyguanosine-malondialdehyde adduct in rat DNA.

作者信息

Draper H H, Agarwal S, Nelson D E, Wee J J, Ghoshal A K, Farber E

机构信息

Department of Nutritional Sciences, University of Guelph, Ontario, Canada.

出版信息

Lipids. 1995 Oct;30(10):959-61. doi: 10.1007/BF02537489.

DOI:10.1007/BF02537489
PMID:8538385
Abstract

The effect of age and peroxidative stress on the concentration of a deoxyguanosine malondialdehyde adduct (dG-MDA) in rat tissues was investigated. Vitamin E deficiency had no effect on the dG-MDA content of liver DNA in rats fed a diet containing 10% corn oil. When 2% cod liver oil was added to this diet, the dG-MDA content of liver DNA doubled in the positive controls fed a high level of vitamin E (100 ppm dl-alpha-tocopherol), and there was a further increase when vitamin E was deleted. Neither iron nitrilotriacetate administration nor choline deficiency had any effect on the dG-MDA content of liver DNA. Carbon tetrachloride had a lowering effect. The failure of iron or carbon tetrachloride administration and of vitamin E deficiency to increase liver dG-MDA is consistent with their failure in previous experiments to affect the urinary excretion of dG-MDA. In contrast, these forms of peroxidative stress produce large increments in the urinary excretion of MDA adducts with lysine, reflecting increased formation and degradation of MDA-modified proteins. DNA appears to be protected from modification by MDA produced at extranuclear sites. The frequency of dG-MDA in different tissues of 4-month-old rats varied markedly: brain >> liver > kidneys and testes. Higher concentrations of dG-MDA were found in the liver and kidneys, but not the testes, of 25-month-old rats. The determinants of the concentration of dG-MDA in DNA merit further investigation.

摘要

研究了年龄和过氧化应激对大鼠组织中脱氧鸟苷丙二醛加合物(dG-MDA)浓度的影响。维生素E缺乏对喂食含10%玉米油饮食的大鼠肝脏DNA的dG-MDA含量没有影响。当在该饮食中添加2%的鳕鱼肝油时,喂食高水平维生素E(100 ppm dl-α-生育酚)的阳性对照中肝脏DNA的dG-MDA含量增加了一倍,而当维生素E缺失时则进一步增加。给予次氮基三乙酸铁或胆碱缺乏对肝脏DNA的dG-MDA含量均无任何影响。四氯化碳有降低作用。给予铁或四氯化碳以及维生素E缺乏未能增加肝脏dG-MDA,这与它们在先前实验中未能影响dG-MDA的尿排泄一致。相比之下,这些形式的过氧化应激会使赖氨酸的MDA加合物的尿排泄大幅增加,反映出MDA修饰蛋白的形成和降解增加。DNA似乎受到保护,免受核外部位产生的MDA的修饰。4月龄大鼠不同组织中dG-MDA的频率差异显著:脑>>肝脏>肾脏和睾丸。在25月龄大鼠的肝脏和肾脏中发现了较高浓度的dG-MDA,但在睾丸中未发现。DNA中dG-MDA浓度的决定因素值得进一步研究。

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本文引用的文献

1
Increased formation and degradation of malondialdehyde-modified proteins under conditions of peroxidative stress.
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2
A comparative evaluation of thiobarbituric acid methods for the determination of malondialdehyde in biological materials.用于测定生物材料中丙二醛的硫代巴比妥酸方法的比较评估。
Free Radic Biol Med. 1993 Oct;15(4):353-63. doi: 10.1016/0891-5849(93)90035-s.
3
Identification of a deoxyguanosine-malondialdehyde adduct in rat and human urine.
Lipids. 1994 Jun;29(6):429-32. doi: 10.1007/BF02537312.
4
甲状腺功能亢进和减退对小鼠骨骼肌脂质过氧化、磷脂不饱和性、谷胱甘肽系统以及核DNA和线粒体DNA氧化损伤的影响。
Mol Cell Biochem. 2001 May;221(1-2):41-8. doi: 10.1023/a:1010930110382.
4
Correlation of fatty acid unsaturation of the major liver mitochondrial phospholipid classes in mammals to their maximum life span potential.哺乳动物肝脏主要线粒体磷脂类脂肪酸不饱和度与其最大寿命潜力的相关性。
Lipids. 2001 May;36(5):491-8. doi: 10.1007/s11745-001-0748-y.
The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens.通过饮食中胆碱和蛋氨酸缺乏且不添加致癌物诱导肝癌
Carcinogenesis. 1984 Oct;5(10):1367-70. doi: 10.1093/carcin/5.10.1367.
5
Unequivocal demonstration that malondialdehyde is a mutagen.
Carcinogenesis. 1983;4(3):331-3. doi: 10.1093/carcin/4.3.331.
6
Probable free radical effects on rat liver nuclei during early hepatocarcinogenesis with a choline-devoid low methionine diet.在胆碱缺乏低蛋氨酸饮食诱导大鼠早期肝癌发生过程中自由基对大鼠肝细胞核可能产生的影响。
Cancer Res. 1987 Dec 15;47(24 Pt 1):6731-40.
7
Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo.尿丙二醛对体内刺激脂质过氧化因素的反应。
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Free Radic Biol Med. 1990;8(1):3-7. doi: 10.1016/0891-5849(90)90137-8.
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Isolation of a malondialdehyde-deoxyguanosine adduct from rat liver DNA.从大鼠肝脏DNA中分离出丙二醛-脱氧鸟苷加合物。
Free Radic Biol Med. 1992 Dec;13(6):695-9. doi: 10.1016/0891-5849(92)90043-g.