Department of Cardiology, Kanazawa Medical University, Ishikawa, Japan.
Department of Forensic Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Scand Cardiovasc J. 2022 Dec;56(1):180-186. doi: 10.1080/14017431.2022.2085884.
. Endothelial dysfunction caused by oxidative stress plays an important role in the development of vasospastic angina pectoris (VSAP). Glutamate causes endothelial dysfunction by generating oxidative stress, and it inhibits cystine import into endothelial cells via the cystine/glutamate antiporter (X), which leads to depletion of antioxidant glutathione. However, whether glutamate and cystine are implicated in the pathogenesis of VSAP remains unclear. We investigated plasma glutamate and cystine levels, oxidative stress markers and antioxidant capacity in non-smoker patients with VSAP to determine whether glutamate and cystine are associated with the development of VSAP. We assessed 49 non-smokers assigned to groups with ( = 27) and without ( = 22) VSAP, and also measured plasma glutamate, cystine, nitrotyrosine, reactive oxygen metabolites and biological antioxidant potential. . Plasma glutamate and cystine values were significantly higher in the group with, than without VSAP (59.8 ± 25.7 vs. 43.5 ± 18.7 µmol/L, = .016 and 35.3 ± 14.2 vs. 25.2 ± 9.1 µmol/L, = .0056, respectively). Plasma glutamate and cystine values were significantly and positively associated ( = 0.32, = .027). Levels of the oxidative stress markers nitrotyrosine and reactive oxygen metabolites, and biological antioxidant potential of as a measure of antioxidant capacity, did not significantly differ between the two groups. However, glutamate and biological antioxidant potential values were significantly and negatively associated ( = -0.3, = .036). . Plasma glutamate levels were increased in patients with VSAP who did not smoke, and they were positively associated with plasma cystine and negatively associated with the biological antioxidant potential levels.
氧化应激引起的内皮功能障碍在血管痉挛性心绞痛（VSAP）的发展中起着重要作用。谷氨酸通过产生氧化应激导致内皮功能障碍，通过胱氨酸/谷氨酸反向转运体（X）抑制胱氨酸进入内皮细胞，导致抗氧化谷胱甘肽耗竭。然而，谷氨酸和胱氨酸是否与 VSAP 的发病机制有关尚不清楚。我们研究了非吸烟者 VSAP 患者的血浆谷氨酸和胱氨酸水平、氧化应激标志物和抗氧化能力，以确定谷氨酸和胱氨酸是否与 VSAP 的发展有关。我们评估了 49 名非吸烟者，分为有（ = 27）和没有（ = 22）VSAP 的两组，并测量了血浆谷氨酸、胱氨酸、硝基酪氨酸、活性氧代谢物和生物抗氧化能力。血浆谷氨酸和胱氨酸值在有 VSAP 的组中明显高于无 VSAP 的组（59.8 ± 25.7 与 43.5 ± 18.7 μmol/L， = .016 和 35.3 ± 14.2 与 25.2 ± 9.1 μmol/L， = .0056，分别）。血浆谷氨酸和胱氨酸值呈显著正相关（ = 0.32， = .027）。两组之间的氧化应激标志物硝基酪氨酸和活性氧代谢物水平以及作为抗氧化能力的生物抗氧化能力没有显著差异。然而，谷氨酸和生物抗氧化能力值呈显著负相关（ = -0.3， = .036）。在不吸烟的 VSAP 患者中，血浆谷氨酸水平升高，与血浆胱氨酸呈正相关，与生物抗氧化能力呈负相关。
