4 research outputs found

    Value of ischemia modified albumin (IMA) for diagnosis of acute coronary syndrome (ACS) in patients with acute chest pain

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    The aim of this study was to evaluate the diagnostic accuracy of ischemia modified albumin (IMA) alone, or in combination with cardiac troponin T (cTnT) and electrocardiogram (ECG) findings for diagnosis of acute coronary syndrome (ACS). The study included patients with acute chest pain suggestive on ACS, recruited within 6 hours from onset. Patients were classified in ACS group and non-ischemic chest pain group (NICP). Of 84 patients, 49 were diagnosed with ACS and 35 with NICP. IMA was significantly higher in ACS group (p<0.0001). The area under receiver operating curve for IMA in ACS diagnosis was 0.95 (p<0.0001). Sensitivity and specificity of IMA for ACS diagnosis were 89.8% and 91.4%, respectively. IMA significantly (p<0.05) improved the sensitivity of ECG and cTnT, alone, and in combination. Sensitivity and negative predictive value of combination of IMA, ECG and cTnT for diagnosis of ACS were 100%. IMA is useful for diagnosis of ACS, in combination with ECG and cTnT

    Reduced glutathione level and gsh-dependent enzyme activities in corticonuclear blocks of lenses in patients with senile cataract

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    Introduction. Reduced compound glutathione (GSH) in the lens has the function to protect the thiol group of lens proteins, and as a substrate of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Protein containing thiol groups is significant for the normal function of lens epithelium, i.e. enzymes Na-K-ATP-ase, thus influencing cell permeability. The relationship GSH/GSSG (oxidized glutathione) is normally high in the lens and other ocular tissue owing to the glutathioneredox cycle, which is localized in the lens epithelium and cortex surface. Objective. The aim of the study was to investigate non-enzymic factors of the antioxidant protection of non-protein and protein tiol, as well as to determine glutathione-dependent enzyme activity in the corticonuclear blocks of lenses in patients with senile cataract. Methods. Biochemical studies of lens were carried on 101 patients with senile cataract. According to cataract maturity degree, the patients were classified into two groups: senile incipient cataract (N=41) and mature senile cataract (N=60). GSH concentration was determined by Ellman’s reagent. GPx activity was assayed with cumene hydroperoxide, and that of glutathione S-transferase by follow-up of glutathione conjugation and 1-chloro-2.4-dinitrobenzene rates. Results. A significantly higher GSH concentration was found in the corticonuclear blocks of lenses with initial as related to mature cataract (p&lt;0.001). The activity of enzyme GPx and GST was considerably higher in the corticonuclear blocks of lenses with initial cataract (p&lt;0.001). With cataract progression, the quantity of available GSH, necessary for GPx and GST functioning, declined, so that the activity of these enzymes was also significantly decreased in mature cataract. Conclusion. The determined lower GSH concentration and antioxidant enzyme activity in corticonuclear blocks of lenses, particularly in cataract with a nuclear component, indicate the weakened antioxidant response of lens tissue during the development of senile cataract

    Examination of myeloperoxidase activity, as an indicator of inflammation in obese participants with metabolic syndrome

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    Introduction. Obesity is a complex metabolic disorder and one of the most common modern health problems. Numerous studies indicate association between chronic low-grade inflammatory state and obesity. Myeloperoxidase (MPO) and its reactive oxidants participate in tissue damage in the course of inflammatory processes. The aim of this study was to examine MPO activity in the serum of obese participants with metabolic syndrome and its relationship with other indicators of inflammation. Material and Methods: Participants were divided into three groups according to the anthropometric parameters and biochemical indicators: normally fed ones (n=30), participants with abdominal obesity (n = 30) and participants with metabolic syndrome (n = 30). In the serum of patients was being determined chlorination activity of MPO by spectrophotometry. Results: Significant differences were found in MPO activity in all three groups of participants such as: the maximum activity was measured in patients with metabolic syndrome (p <0.001). There was a positive correlation between MPO activity and atherogenic index, as well as between the MPO and the concentration of LDL-cholesterol, while the negative correlation was found between MPO and the concentration of HDL-cholesterol. Conclusion: The examination has shown that the activity of MPO progressively increases with obesity and metabolic syndrome. The obtained results suggest that MPO can be of great importance for the pathophysiological mechanisms leading to the development of complications of obesity and metabolic syndrome

    The Role of Oxidative Stress in the Onset and Development of Age-Related Macular Degeneration

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    Age-related macular degeneration (AMD) is a complex, degenerative and progressive chronic disease that leads to severe visual loss. The prevalence of early AMD accounts for 18% in the population between 65 and 74 years of age and even 30% in subjects older than 74 years. The articles published in the last decade point out to a significant role of oxidative stress in the onset and development of age-related macular degeneration. Generally, reactive oxygen species (ROS) are produced in the eye during light absorption and physiological metabolic processes. The level of oxidative stress is kept under control by the action of antioxidants and reparative enzymes. Excessive synthesis of ROS leads to increased oxidative modification of lipids, proteins and DNA, causing oxidative damage of cytoplasmic and nuclear cell elements and changes of the extracellular matrix. The accumulation of oxidatively modified compounds in drusen deposits will initiate the onset and development of AMD. The objective of this review was to highlight the mechanisms of oxidative stress in order to elucidate their significance and association with the pathogenesis of AMD
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