Gómez-Amores Lucía, Mate Alfonso, Revilla Elisa, Santa-María Consuelo, Vázquez Carmen M
Department of Physiology and Zoology, Faculty of Pharmacy, University of Seville, C/Profesor García González 2, E-41012 Seville, Spain.
Life Sci. 2006 Mar 20;78(17):1945-52. doi: 10.1016/j.lfs.2005.08.023. Epub 2005 Nov 2.
Oxidative stress plays an important role in arterial hypertension and propionyl-L-carnitine (PLC) has been found to protect cells from toxic reactive oxygen species. In this work, we have evaluated the antioxidant capacity of chronic PLC treatment in spontaneously hypertensive rats (SHR) by measuring the activity of antioxidant enzymes and the lipid peroxidation in liver and cardiac tissues. The activity of glutathione peroxidase was decreased in liver and cardiac tissues of SHR when compared with their normotensive controls, Wistar- Kyoto (WKY) rats, this alteration being prevented by PLC treatment. Glutathione reductase activity was increased in hypertensive rats and no effect was observed after the treatment. No significant changes in superoxide dismutase activity were observed among all experimental groups. Liver of hypertensive rats showed higher catalase activity than that of normotensive rats, and PLC enhanced this activity in both rat strains. Thiobarbituric acid reactive substances, determined as a measure of lipid peroxidation, were increased in SHR compared with WKY rats, and PLC treatment decreased these values not only in hypertensive rats but also in normotensive ones. The content of carnitine in serum, liver and heart was higher in PLC-treated rats, but PLC did not prevent the hypertension development in young SHR. In addition, triglyceride levels, which were lower in SHR than WKY rats, were reduced by chronic PLC treatment in both rat strains. These results demonstrate: i) the hypotriglyceridemic effect of PLC and ii) the antioxidant capacity of PLC in SHR and its beneficial use protecting tissues from hypertension-accompanying oxidative damage.
氧化应激在动脉高血压中起重要作用,并且已发现丙酰 - L - 肉碱(PLC)可保护细胞免受有毒活性氧的损伤。在本研究中,我们通过测量抗氧化酶活性以及肝脏和心脏组织中的脂质过氧化,评估了慢性PLC治疗对自发性高血压大鼠(SHR)的抗氧化能力。与正常血压对照Wistar - Kyoto(WKY)大鼠相比,SHR肝脏和心脏组织中的谷胱甘肽过氧化物酶活性降低,而PLC治疗可预防这种改变。高血压大鼠的谷胱甘肽还原酶活性增加,治疗后未观察到影响。所有实验组中超氧化物歧化酶活性均未观察到显著变化。高血压大鼠肝脏的过氧化氢酶活性高于正常血压大鼠,并且PLC增强了两种大鼠品系中的该活性。作为脂质过氧化指标测定的硫代巴比妥酸反应性物质在SHR中比WKY大鼠增加,并且PLC治疗不仅降低了高血压大鼠的这些值,也降低了正常血压大鼠的这些值。PLC处理的大鼠血清、肝脏和心脏中的肉碱含量较高,但PLC并未阻止年轻SHR的高血压发展。此外,SHR中低于WKY大鼠的甘油三酯水平在两种大鼠品系中均通过慢性PLC治疗而降低。这些结果表明:i)PLC的降甘油三酯作用;ii)PLC在SHR中的抗氧化能力及其在保护组织免受高血压伴随的氧化损伤方面的有益用途。