Islam Rahib K, Donnelly Erinn, Islam Kazi N
LSU Health Sciences Center, Department of Pharmacology, 1901 Perdido St., New Orleans, LA 70112, USA.
Agricultural Research Development Program, College of Engineering, Science, Technology and Agriculture, Central State University, 1400 Brush Row Road, Wilberforce, OH 45384, USA.
J Clin Med. 2021 Sep 28;10(19):4460. doi: 10.3390/jcm10194460.
Human immunodeficiency virus (HIV) attacks the immune system and weakens the ability to fight infections/disease. Furthermore, HIV infection confers approximately two-fold higher risk of cardiac events compared with the general population. The pathological mechanisms responsible for the increased incidence of cardiovascular disease in HIV patients are largely unknown. We hypothesized that increased oxidative stress and attenuated circulating levels of the cardioprotective gaseous signaling molecules, nitric oxide (NO), and hydrogen sulfide (HS) were involved in the cardiovascular pathobiology observed in HIV patients. Plasma samples from both HIV patients and age-matched normal subjects were used for all assays. Oxidative stress was determined by analyzing the levels of advanced oxidation protein products (AOPP) and HO. Antioxidant levels were determined by measuring the levels of trolox equivalent capacity. ADMA, hs-CRP, and IL-6 were determined by using ELISA. The levels of HS (free HS and sulfane sulfur) and NO (nitrite) were determined in the plasma samples by using gas chromatography and HPLC, respectively. In the present study we observed a marked induction in the levels of oxidative stress and decreased antioxidant status in the plasma of HIV patients as compared with the controls. Circulating levels of the cardiovascular disease biomarkers: ADMA, hs-CRP (high-sensitivity C-reactive protein), and IL-6 were significantly increased in the circulatory system of HIV patients. The levels of both nitrite and HS/sulfane sulfur were significantly reduced in the plasma of HIV patients as compared with normal subjects. Our data demonstrate significant increases in circulating biomarkers of oxidative stress and cardiovascular (CV) in conjunction with decreased bioavailability of HS and NO in HIV patients. Diminished levels of these two cardioprotective gaseous signaling molecules may be involved in the pathogenesis of CV disease in the setting of HIV.
人类免疫缺陷病毒（HIV）会攻击免疫系统，削弱机体抵抗感染/疾病的能力。此外，与普通人群相比，HIV感染使心脏事件的风险增加约两倍。HIV患者心血管疾病发病率增加的病理机制在很大程度上尚不清楚。我们推测，氧化应激增加以及具有心脏保护作用的气体信号分子一氧化氮（NO）和硫化氢（HS）的循环水平降低与HIV患者所观察到的心血管病理生物学有关。HIV患者和年龄匹配的正常受试者的血浆样本用于所有检测。通过分析晚期氧化蛋白产物（AOPP）和HO的水平来确定氧化应激。通过测量特罗洛克斯等效容量水平来确定抗氧化剂水平。使用酶联免疫吸附测定法（ELISA）测定不对称二甲基精氨酸（ADMA）、高敏C反应蛋白（hs-CRP）和白细胞介素-6（IL-6）。分别使用气相色谱法和高效液相色谱法测定血浆样本中HS（游离HS和硫烷硫）和NO（亚硝酸盐）的水平。在本研究中，我们观察到与对照组相比，HIV患者血浆中的氧化应激水平显著升高，抗氧化状态降低。HIV患者循环系统中心血管疾病生物标志物ADMA、hs-CRP（高敏C反应蛋白）和IL-6的循环水平显著升高。与正常受试者相比，HIV患者血浆中亚硝酸盐和HS/硫烷硫的水平均显著降低。我们的数据表明，HIV患者氧化应激和心血管（CV）循环生物标志物显著增加，同时HS和NO的生物利用度降低。这两种具有心脏保护作用的气体信号分子水平降低可能参与了HIV感染情况下CV疾病的发病机制。
