Oxidative stress is a "privilege" of aerobic organisms. It can be induced by endogenous and exogenous factors. Most often, it is characterized by the production of free radicals and nonradical oxygen and nitrogen products, referred to under a single term "reactive species" (RS). Oxidative stress is a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins and DNA. However, reactive oxygen (ROS) and nitrogen species (RNS) are "two-faced" products. Produced in low/moderate concentrations as molecular signals that regulate a series of physiological processes, such as a defence against infectious agents, the maintenance of vascular tone, the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. Many of ROS-mediated responses protect cells against oxidative stress and maintain "redox homeostasis". Then, both reactive species are produced by strictly regulated enzymes, such as nitric oxide synthase (NOS), and isoforms of NADPH oxidase, or as by-products from not so well regulated sources, such as the mitochondrial electron-transport chain. An excessive increase in ROS production has been implicated in the pathogenesis of atherosclerosis, cardiovascular diseases, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative and immuno-inflammatory diseases. Within the cells, ROS can act as secondary messengers in intracellular signalling cascades, which can induce the oncogenic phenotype of cancer cells, cellular senescence and apoptosis.
The role of the oxidative stress in cataractogenesis could not be the same for all cataract types. High level of lipid peroxides in pigmented cataracts may point to the different nature of pigment source than proteins solely, whereas lipid peroxidation and SH groups consumption in cortical cataractogenesis might be of less importance.
The obtained results showed that apoptotic process is dysregulated in the patients with ischemic heart disease. Interdependence between Fas and FasL and inflammatory and lipid markers as well as with cardiovascular risk factors was established.
The results of this study suggest that in stable angina patients, if studied over time, serum neopterin or NO2(-)/NO3(-) levels may indicate future plaque instability. In ST-elevation myocardial infarction patients, neopterin and/or NO2(-)/NO3(-) levels may identify patients at long-term risk of death or recurrent acute coronary events after myocardial infarction.
Increased galectin-3 plasma concentration has been linked to an unfavorable outcome in patients with heart failure or atrial fibrillation (AF). There are no published data about the prognostic utility of galectin-3 and high-sensitivity C-reactive protein (hs-CRP) for long-term clinical outcome in the Non-ST elevation acute myocardial infarction (NSTEMI) patients with preexisting AF. Thirty-two patients with the first acute NSTEMI and preexisting AF and 22 patients without preexisting AF, were prospectively followed for fifteen months. Patients with AF had significantly higher galectin-3 plasma levels (p < 0.05) and hs-CRP concentration (p < 0.01), compared with patients without AF. Galectin-3 plasma concentration was not a significant covariate of the composite outcomes (p = 0.913). Patients with high hs-CRP (above 4.55 mg/L) showed 2.5 times increased risk (p < 0.05) of the composite outcome occurrence (p < 0.05). Besides, three-vessel coronary artery disease, creatinine serum level, and creatinine clearance were significant covariates (p < 0.05; p < 0.05; p < 0.01) of the composite outcome, respectively. Creatinine clearance, solely, has been shown to be an independent predictor of unfavorable prognosis after a 15-month follow-up. Galectin-3 and hs-CRP plasma levels were elevated in NSTEMI patients with AF, but with differential predictive value for an unfavorable clinical outcome. Only hs-CRP was associated with increased risk of composite outcome occurrence.
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