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[磷酸吡哆醛恢复老年动物心脏和血管组织中硫化氢合成及氧化还原状态]

[PYRIDOXAL-5-PHOSPHATE RESTORES HYDROGEN SULFIDE SYNTHES AND REDOX STATE OF HEART AND BLOOD VESSELS TISSUE IN OLD ANIMALS].

作者信息

Mys L A, Budko A Yu, Strutynska N A, Sagach V F

出版信息

Fiziol Zh (1994). 2017;63(1):3-9. doi: 10.15407/fz63.01.003.

Abstract

It was shown the alterations in hydrogen sulfide (H(2)S) metabolism and the development of oxidative and nitrozative stress in cardiovascular system by aging. The administration of pyridoxal-5-phosphate as cofactor of H(2)S synthesizing enzymes restored endogenous H(2)S level and redox state in the heart and aorta tissues. Under these conditions, the following indicators of oxidative stress were significantly decreased in heart and aorta tissues: superoxide generation rate (·0(2)(-)) and hydroxyl (·OH) anion radicals, compared with significantly elevated levels of these parameters in old animals. We also found the reduction of non-enzymatic (diene conjugates and malonic dialdehyde) and enzymatic (uric acid, LTC(4) and TxB(2)) lipid oxidation products levels in old rats under H(2)S synthesis stimulation that confirms the restriction of oxidative stress. An important consequence of endogenous synthesis stimulation of hydrogen sulfide during aging is a decrease of nitrozative stress, such as iNOS activity and nitrate reductase, as well as recovery of constitutive NO synthase activity, indicating the importance of this gas transmitter in cardiovascular system. Thus, stimulation of hydrogen sulfide endogenous synthesis contributed to reduced production of reactive oxygen species (oxidative stress) and nitrogen (nitrozative stress) in heart and aorta tissues with aging. The presence of a pronounced antioxidant effect and modulating influence of pyridoxal-5- phosphate in the redox state of heart tissue and blood vessels during aging suggests cardioprotective properties of the substance and prospects for future research.

摘要

研究表明,衰老会导致心血管系统中硫化氢(H₂S)代谢改变以及氧化应激和亚硝化应激的发展。给予磷酸吡哆醛作为H₂S合成酶的辅因子可恢复心脏和主动脉组织中的内源性H₂S水平和氧化还原状态。在这些条件下,与老年动物中这些参数显著升高的水平相比,心脏和主动脉组织中氧化应激的以下指标显著降低:超氧化物生成速率(·O₂⁻)和羟基(·OH)阴离子自由基。我们还发现,在H₂S合成刺激下,老年大鼠中非酶促(二烯共轭物和丙二醛)和酶促(尿酸、LTC₄和TxB₂)脂质氧化产物水平降低,这证实了氧化应激受到限制。衰老过程中内源性硫化氢合成刺激的一个重要结果是亚硝化应激降低,如诱导型一氧化氮合酶活性和硝酸还原酶,以及组成型一氧化氮合酶活性的恢复,表明这种气体递质在心血管系统中的重要性。因此,内源性硫化氢合成的刺激有助于减少衰老过程中心脏和主动脉组织中活性氧(氧化应激)和氮(亚硝化应激)的产生。磷酸吡哆醛在衰老过程中对心脏组织和血管的氧化还原状态具有显著的抗氧化作用和调节影响,这表明该物质具有心脏保护特性以及未来研究的前景。

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