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维生素 A 补充不同时间改变大鼠血管氧化还原参数。

Vitamin A supplementation for different periods alters rat vascular redox parameters.

机构信息

Center of Oxidative Stress Research, Professor Tuiskon Dick Department of Biochemistry, Institute of Health Basic Sciences (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, Brazil.

出版信息

J Physiol Biochem. 2010 Dec;66(4):351-7. doi: 10.1007/s13105-010-0041-7. Epub 2010 Aug 19.

DOI:10.1007/s13105-010-0041-7
PMID:20721707
Abstract

Vitamin A plays physiological and antioxidants properties and is associated with protective effects on arterial level. However, deleterious effects have been reported, including those observed by our group, which has demonstrated pro-oxidant properties in other systems. Therefore, it is needed to better understand the redox effects of retinoids on arterial system. Thus, our aim was to compare vascular redox parameters among animals supplemented or not with vitamin A. Eighty-five adult male rats were treated with different retinyl palmitate doses (1,000-9,000 IU kg(-1) day(-1)) or saline for 3 (25 rats, n=5 for each group), 7 (25 rats, n=5 for each group), and 28 (35 rats, n=7 for each group) days periods. Aorta artery was surgically removed, cleaned to remove the blood, and homogenized. It was evaluated thiobarbituric reactive species (TBARS), total reduced sulfhydryl (SH), and activities of superoxide dismutase (SOD) and catalase (CAT). Statistics were conducted by one-way ANOVA with Dunnet's post hoc and significance value of p≤0.05. About TBARS, we observed no modifications after 3 days, but a decrease after 7 days in all doses and after 28 days in three higher doses. The two higher doses yielded an increase on SH only after 3 days. SOD activity decreased in three higher doses after 3 days and in all doses after 28 days, but no modifications after 7 days, while CAT activity increased in all doses after 3 days, decreased in all doses after 7 days, and did not change after 28 days. In conclusion, vitamin A induces antioxidant status on vascular level.

摘要

维生素 A 具有生理和抗氧化特性,与动脉水平的保护作用有关。然而,已经报道了有害作用,包括我们小组观察到的那些,我们的小组已经在其他系统中证明了其具有促氧化剂特性。因此,需要更好地了解类视黄醇对动脉系统的氧化还原作用。因此,我们的目的是比较补充或不补充维生素 A 的动物的血管氧化还原参数。85 只成年雄性大鼠用不同的视黄醇棕榈酸酯剂量(1000-9000 IU/kg/天)或生理盐水处理 3(25 只大鼠,每组 5 只)、7(25 只大鼠,每组 5 只)和 28(35 只大鼠,每组 7 只)天。手术切除主动脉,清除血液,匀浆。评估了硫代巴比妥酸反应性物质(TBARS)、总还原巯基(SH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。采用单因素方差分析和 Dunnett 事后检验进行统计学分析,显著性水平为 p≤0.05。关于 TBARS,我们观察到 3 天后没有变化,但 7 天后所有剂量都减少,28 天后三个更高剂量减少。前两个更高剂量仅在 3 天后增加 SH。SOD 活性在三个更高剂量的 3 天后和所有剂量的 28 天后下降,但 7 天后没有变化,而 CAT 活性在所有剂量的 3 天后增加,在所有剂量的 7 天后下降,28 天后没有变化。总之,维生素 A 在血管水平诱导抗氧化状态。

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本文引用的文献

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Long-term vitamin A supplementation at therapeutic doses induces mitochondrial electrons transfer chain (METC) impairment and increased mitochondrial membrane-enriched fraction (MMEF) 3-nitrotyrosine on rat heart.长期给予治疗剂量的维生素 A 补充会导致大鼠心脏中线粒体电子传递链(METC)损伤和富含线粒体膜的部分(MMEF)3-硝基酪氨酸增加。
Free Radic Res. 2010 May;44(5):505-12. doi: 10.3109/10715761003636849.
2
Vitamin A supplementation at pharmacological doses induces nitrosative stress on the hypothalamus of adult Wistar rats.以药理剂量补充维生素A会在成年Wistar大鼠的下丘脑诱导氧化应激。
Chem Biol Interact. 2009 Aug 14;180(3):407-13. doi: 10.1016/j.cbi.2009.02.006. Epub 2009 Feb 23.
3
Retinoids as critical modulators of immune functions: new therapeutic perspectives for old compounds.
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Endocr Metab Immune Disord Drug Targets. 2009 Jun;9(2):113-31. doi: 10.2174/187153009788452435.
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Evaluation of redox and bioenergetics states in the liver of vitamin A-treated rats.维生素A处理大鼠肝脏中氧化还原和生物能量状态的评估。
Eur J Pharmacol. 2009 May 21;610(1-3):99-105. doi: 10.1016/j.ejphar.2009.03.046. Epub 2009 Mar 24.
5
The NF kappa B-mediated control of RS and JNK signaling in vitamin A-treated cells: duration of JNK-AP-1 pathway activation may determine cell death or proliferation.维生素A处理的细胞中NF-κB介导的RS和JNK信号传导控制:JNK-AP-1途径激活的持续时间可能决定细胞死亡或增殖。
Biochem Pharmacol. 2009 Apr 1;77(7):1291-301. doi: 10.1016/j.bcp.2008.12.010. Epub 2008 Dec 31.
6
Short-term vitamin A supplementation at therapeutic doses induces a pro-oxidative state in the hepatic environment and facilitates calcium-ion-induced oxidative stress in rat liver mitochondria independently from permeability transition pore formation : detrimental effects of vitamin A supplementation on rat liver redox and bioenergetic states homeostasis.短期给予治疗剂量的维生素 A 补充剂会在肝内环境中诱导出一种促氧化状态,并独立于通透性转换孔形成促进钙离子诱导的大鼠肝线粒体氧化应激:维生素 A 补充对大鼠肝内氧化还原和生物能量状态平衡的有害影响。
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