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

L A Mys, A Yu Budko, N A Strutynska, V F Sagach
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引用次数: 7

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.

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[吡哆醛-5-磷酸恢复老年动物心脏和血管组织的硫化氢合成和氧化还原状态]。
结果表明,随着年龄的增长,心血管系统硫化氢(H(2)S)代谢发生改变,氧化应激和硝态应激发生变化。吡哆醛-5-磷酸作为H(2)S合成酶的辅助因子,可恢复心脏和主动脉组织内源性H(2)S水平和氧化还原状态。在这些条件下,心脏和主动脉组织的氧化应激指标:超氧化物生成率(·0(2)(-))和羟基(·OH)阴离子自由基显著降低,而老龄动物的这些指标均显著升高。我们还发现,在H(2)S合成刺激下,老龄大鼠的非酶促(二烯偶联物和丙二醛)和酶促(尿酸、LTC(4)和TxB(2))脂质氧化产物水平降低,证实了氧化应激的限制。在衰老过程中,内源性硫化氢合成刺激的一个重要结果是一氧化氮(iNOS)活性和硝酸还原酶等氮化应激的降低,以及组成型一氧化氮合酶活性的恢复,这表明了这种气体递质在心血管系统中的重要性。因此,刺激硫化氢内源性合成有助于减少心脏和主动脉组织中活性氧(氧化应激)和氮(氮化应激)的产生。在衰老过程中,吡哆醛-5-磷酸在心脏组织和血管氧化还原状态中具有明显的抗氧化作用和调节作用,这表明该物质具有保护心脏的特性,并为未来的研究提供了前景。
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