Department of Animal Physiology, Institute of Biology, Pomeranian University in Słupsk, Arciszewski St. 22b, PL 76-200 Słupsk, Poland.
Department of Ecology, Geography and Nature Management, T.H. Shevchenko National University "Chernihiv Colehium", Hetmana Polubotka St. 53, 14013 Chernihiv, Ukraine.
Int J Mol Sci. 2024 Nov 18;25(22):12364. doi: 10.3390/ijms252212364.
The aim of this study was to evaluate the combined effects of L-arginine, intermittent hypoxia training (IHT), and acute stress on oxygen-dependent processes in rats, including mitochondrial oxidative phosphorylation, microsomal oxidation, and the intensity of lipoperoxidation processes. In addition, our study investigated how the modulatory effect of the NO synthase mechanism on the concentration of catecholamines (CA), such as adrenaline and noradrenaline, and their biosynthetic precursors (DOPA, dopamine) varies depending on the cholinergic (acetylcholine, Ach-acetylcholinesterase, AChE) status in rats. This study investigated the protective stress-limiting effects of L-arginine impact and IHT in the blood and liver of rats. The results showed that L-arginine promoted the maintenance of NAD-dependent oxidation in mitochondria, which was detrimental compared to succinate oxidation, and was accompanied by depletion of respiratory activity reserves under stress induced by high concentrations of CA. The interdependence of SC-dependent oxidation and the functional role of NAD-dependent substrate oxidation in the mitochondrial respiratory chain in stress conditions induced using inhibitors revealed the importance of the NO system. Administration of L-arginine during the IHT course prior to stress exposure increased the compensatory capacity of the organism. L-arginine increased the compensatory capacity of the sympathoadrenal system in stress-exposed rats. In the early stages of IHT, modulation of the CA concentration was observed with a concomitant increase in lipoperoxidation processes, and in the final stages of IHT, the CA concentrations increased, but there was also an inhibition of lipoperoxidation, which was particularly enhanced by the administration of L-arginine. The increase in blood concentrations of CA and ACh was accompanied by a decrease in AChE activity at different stages of adaptation to hypoxia induced by IHT (days 5, 10, and 14). Thus, the IHT method significantly mobilises the reserve capacity of oxygen-dependent processes through the system of CA, ACh-AChE mediated by nitric oxide.
本研究旨在评估 L-精氨酸、间歇性低氧训练 (IHT) 和急性应激对大鼠氧依赖过程的综合影响，包括线粒体氧化磷酸化、微粒体氧化和脂质过氧化过程的强度。此外，我们的研究还探讨了一氧化氮合酶机制对儿茶酚胺 (CA) 浓度的调节作用如何变化，例如肾上腺素和去甲肾上腺素，以及它们的生物合成前体（DOPA、多巴胺），这取决于大鼠的胆碱能（乙酰胆碱、Ach-乙酰胆碱酯酶、AChE）状态。本研究探讨了 L-精氨酸对大鼠血液和肝脏的应激限制保护作用以及 IHT 的影响。结果表明，L-精氨酸促进了 NAD 依赖的线粒体氧化，与琥珀酸氧化相比，这是有害的，并且在高浓度 CA 诱导的应激下，呼吸活性储备耗尽。在使用抑制剂诱导的应激条件下，SC 依赖的氧化与 NAD 依赖的底物氧化在线粒体呼吸链中的功能关系揭示了 NO 系统的重要性。在暴露于应激之前的 IHT 过程中给予 L-精氨酸增加了机体的补偿能力。L-精氨酸增加了应激暴露大鼠交感肾上腺系统的补偿能力。在 IHT 的早期阶段，观察到 CA 浓度的调制伴随着脂质过氧化过程的增加，而在 IHT 的最后阶段，CA 浓度增加，但脂质过氧化也受到抑制，特别是通过给予 L-精氨酸增强。血液中 CA 和 ACh 的浓度增加伴随着不同阶段适应 IHT 诱导的低氧时 AChE 活性的降低（第 5、10 和 14 天）。因此，IHT 方法通过 CA、ACh-AChE 介导的一氧化氮系统显著调动了氧依赖过程的储备能力。
