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Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction.

100%
Kalinowski L., Malinski T.
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vol. 51
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issue 2
459-469
EN
There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in endothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2̇̄). Because O2̇̄ rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2̇̄, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2̇̄ in the endothelial cells. It seems that O2̇̄ generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2̇̄. That is maintained at diverse levels.
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Inflammatory response to a marathon run in amateur athletes

52%
Kaleta-Duss A. M., Lewicka-Potocka Z., Dąbrowska-Kugacka A., Raczak G., Siekierzycka A., Woźniak M., Kalinowski L., Lewicka E. K.
European Journal of Translational and Clinical Medicine
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2021
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vol. 4
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issue 1
43-49
EN
Background: While moderate physical exercise has positive effects on the cardiovascular system, the data regarding intensive endurance sports is biased with studies suggesting that the inflammatory response to strenuous exercise may act proarrhythmogenic. In amateurs, the effects of intensive endurance exercise on the cardiovascular system have not been studied. Analysis of the effects of a marathon on the kinetics of inflammatory biomarkers may bring new insights into this issue. Material and methods: We studied the effect of a marathon on the kinetics of inflammatory biomarkers: Endothelin-1 (ET-1), Pentraxin-3 (PTX-3), Neopterin and Interleukin-6 (IL-6) in the population of 35 amateur male marathoners. The study was divided into 3 stages: two weeks prior to the marathon (S1), at the finish line (S2) and two weeks after (S3). Blood analyses for biomarkers were performed at each stage. Results: The concentrations of ET-1 (3.20 ± 0.90 vs. 1.30 ±0.34 pg/ml, p <0,001), PTX-3 (441.09 ± 295.64 vs. 279.99 ± 125.68 pg/ml, p < 0,001), Neopterin (9.97 ± 2.17 vs. 8.36 ± 2.68 nmol/l, p < 0,05) and IL-6 (32.5 ± 13.90 vs. 0.97 ± 0.77 pg/ml, p < 0,001) were significantly higher at S2 compared to S1. Conclusions: Running a marathon causes an acute rise in concentrations of inflammatory biomarkers. Further research is needed on the long-term effects of intensive endurance exercise on the cardiovascular system.
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