BACKGROUND:At the present time the alternation of the oxidative metabolism is considered as one of the leading pathogenic mechanisms in the development and progression of community-acquired pneumonia (CAP). However the nature and direction of the oxidative protein changes in CAP patient’s blood had been almost unexplored.AIM:To define oxidative and modified proteins in erythrocytes and blood plasma of CAP patients.MATERIAL AND METHODS:Blood plasma and erythrocytes obtained from: 42 patients with moderate severity pneumonia, 12 patients with grave severity pneumonia and 32 healthy volunteers. Content of advanced oxidation protein products, malondialdehyde and reactive carbonyl derivatives were estimated as indicators of the oxidative stress and oxidative damage of proteins.RESULTS:In patients with grave severity the level of oxidative proteins and MDA in erythrocytes exceeded both: control values and similar meanings in CAP patients with moderate severity. The further growth of MDA in this group patients’ blood plasma was observed, but the level of oxidative proteins decreased in comparison with those in CAP patients with moderate severity.CONCLUSION:To sum up, our derived data show, that injury of erythrocytes’ redox-status and blood plasma components plays an essential role in development and progression CAP.
At the present time, available views show our limited knowledge of the peculiarities of the functional status of neutrophils and their metabolism in patients with community-acquired pneumonia (CAP). The studying of changes of metabolic status of neutrophils can broaden our views about pneumonia pathogenesis and define datum points of therapeutic effect.
Purpose of our research: to define oxidative stress activity and the level of oxidative modification of proteins of neutrophils in CAP patients.
Materials and methods: neutrophils obtained from 23 patients with community-acquired pneumonia. Control group consisting of 19 healthy volunteers. The reactive carbonyl derivatives of proteins and advanced oxidation protein products were defined so as to assess the oxidative damage of proteins. The malondialdehyde and nitrite ions were assessed as being indicators of the oxidative stress. The neutrophils of CAP patients with moderate severity were characterized by a tendency of evidencing decreasing content of advanced oxidation protein products, along with the statistically important enhanced levels of carbonyl derivatives and nitrite ions, while their malondialdehyde status practically leveled off with the control and had only an insignificant trend towards growth. We have demonstrated the accumulation of carbonyl derivatives and nitrite ions in the peripheral neutrophils of CAP patients. These results give evidence of an oxidative misbalance in the cells which contributes to the aggravation of the disease.
BACKGROUND: Drug-induced kidney disorder is a frequent adverse event which contributes to morbidity and even incapacitation. Our current knowledge of drug-induced kidney disease is limited due to varying definitions of kidney injury, incomplete assessment of concurrent risk factors, and lack of long term outcome reporting.
AIM: The discovery and development of novel biomarkers and local (renal) response mechanisms, which can diagnose kidney damage earlier and more accurately, are needed for effective prevention of drug-induced nephrotoxicity.
METHODS: Forty patients from 22 to 50 years old with drug-induced nephropathy (43 females, 27 males) were included in the study. The determination of oxidative stress modifications as advanced oxidation protein products (AOPPs), protein reactive carbonyl derivatives (PRCD), methylglyoxal, and catalase (CAT) level were assayed. AOPP was rated in blood plasma through the Witko-Sarsat (1996) method, PRCD by Levine (2000) method, methylglyoxal through the Racker (1963) method, CAT was evaluated with Koroljuk (1988) and Aebi (1984) methods. Conditionally, 30 healthy-matched persons were included in the control group.
RESULTS: In psychotropic and nonsteroidal anti-inflammatory drugs (NSAID) drug-induced nephropathy patients, there was a tendency to increase the concentration of AOPP in blood plasma, PRCD, and methylglyoxal in erythrocytes relative to the upper limits of normal ranges. Moreover, there was a significant decrease of the CAT level in blood plasma relative to the upper limits of normal ranges.
CONCLUSION: Thus, the results of the present study permit us to draw the following conclusions. The patients with psychotropic and NSAIDs drug-induced nephropathy have increased level of oxidative stress products and increased neutrophil gelatinase-associated lipocalin level even in normal eGFR. The mechanisms that lead to the development of oxidative stress and the production of modified proteins are different in patients treated with different drugs.
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