Soto María Elena, Manzano-Pech Linaloe, Guarner-Lans Verónica, Rodríguez-Zanella Hugo, Pérez-Torres Israel, Soria-Castro Elizabeth
Research Direction, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, México City 14080, Mexico.
Cardiovascular Line American British Cowdray Medical Center, Sur 136 Numero 116 Col Álvaro Obregón, México City 01120, Mexico.
Diagnostics (Basel). 2024 Dec 13;14(24):2807. doi: 10.3390/diagnostics14242807.
Infective endocarditis (IE) most commonly results from infections by Gram-positive bacteria, and, in this condition, the redox homeostasis is lost due to the overproduction of HO, leading to the overstimulation of the immune system and the upregulation of the production of proinflammatory cytokines. The aim of this study was to evaluate the levels of oxidative biomarkers and the enzymatic and non-enzymatic antioxidant systems in subjects with IE. The study included three cases with IE that had undergone aortic valve replacement (AVR) surgery that was complicated by IE, comparing them with subjects with AVR without IE. We determined the malondialdehyde (MDA), total antioxidant capacity (TAC), carbonyl group concentration, glutathione (GSH), thiols and the nitrate/nitrite ratio (NO/NO) in homogenized tissue from the cardiac valves. We also measured the activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR) and thioredoxin reductase (TrxR). The superoxide dismutase (SOD) isoforms and peroxidase activity were determined using native gels. There were increases in the activity of antioxidant enzymes such as GST, SOD isoforms and peroxidases ( ≤ 0.01) and decreases in oxidative stress markers such as GSH ( = 0.05); meanwhile, MDA and carbonylation were increased ( ≤ 0.05). The results suggest that bacterial infections favor oxidative stress in the aortic valves, which increases the SOD isoforms and peroxidase activity. This contributes to the loss of the intricate redox homeostasis system in patients with IE, causing a positive feedback loop in the oxidative background that results in damage to the heart, likely leading to a fatal outcome.
感染性心内膜炎（IE）最常见的病因是革兰氏阳性菌感染，在此情况下，由于羟基自由基（HO）的过度产生，氧化还原稳态丧失，导致免疫系统过度刺激和促炎细胞因子产生上调。本研究的目的是评估IE患者氧化生物标志物水平以及酶促和非酶促抗氧化系统。该研究纳入了3例因IE并发而接受主动脉瓣置换（AVR）手术的IE患者，并将其与未患IE的AVR患者进行比较。我们测定了来自心脏瓣膜的匀浆组织中的丙二醛（MDA）、总抗氧化能力（TAC）、羰基浓度、谷胱甘肽（GSH）、硫醇以及硝酸盐/亚硝酸盐比率（NO/NO）。我们还测量了谷胱甘肽-S-转移酶（GST）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）和硫氧还蛋白还原酶（TrxR）的活性。使用天然凝胶测定超氧化物歧化酶（SOD）同工型和过氧化物酶活性。抗氧化酶如GST、SOD同工型和过氧化物酶的活性增加（P≤0.01），而氧化应激标志物如GSH降低（P = 0.05）；同时，MDA和羰基化增加（P≤0.05）。结果表明，细菌感染有利于主动脉瓣中的氧化应激，这会增加SOD同工型和过氧化物酶活性。这导致IE患者复杂的氧化还原稳态系统丧失，在氧化背景下形成正反馈回路，从而导致心脏损伤，可能导致致命后果。
