The main purpose of this study was to investigate how extreme physical strain influences cytokine response and oxidative stress markers by examining professional judo athletes during a typical 3-day judo training session (randori combat training).Creatine kinase (CK) activity, a marker of muscle damage, was considerably elevated immediately after randori training. Pro- (IL-1β and TNF-α) and anti-inflammatory (IL-6 and IL-10) cytokines were also increased. The strongest effect was seen in IL-1β concentration, which correlated with CK activity (r = 0.49, P < 0.05). All the observed cytokines returned to baseline (IL-1β) or even dropped below initial levels (TNF-α, IL-6 and IL-10) 12 h after completing the training. Lipid peroxides (LPO), a marker of reactive oxygen species, also decreased below their initial values. LPO levels correlated directly with IL-1β, TNF-α, IL-6 and IL-10.This study is the first to evaluate the effect of a 3-day judo training session on muscle damage by evaluating the release of pro- and anti-inflammatory cytokines and markers of oxidative stress. It is also the first to demonstrate significant changes in the blood cytokine profile that correlate with lipid peroxide levels and muscle damage.
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There is growing evidence that proteins are early targets of reactive oxygen species, and that the altered proteins can in turn damage other biomolecules. In this study, we measured the effects of proteins on the oxidation of liposome phospholipid membranes, and the formation of protein hydroperoxides in serum and in cultured cells exposed to radiation-generated hydroxyl free radicals. Lysozyme, which did not affect liposome stability, gave 50% protection when present at 0.3 mg/ml, and virtually completely prevented lipid oxidation at 10 mg/ml. When human blood serum was irradiated, lipids were oxidized only after the destruction of ascorbate. In contrast, peroxidation of proteins proceeded immediately. Protein hydroperoxides were also generated without a lag period in hybrid mouse myeloma cells, while at the same time no lipid peroxides formed. These results are consistent with the theory that, under physiological conditions, lipid membranes are likely to be effectively protected from randomly-generated hydroxyl radicals by proteins, and that protein peroxyl radicals and hydroperoxides may constitute an important hazard to biological systems under oxidative stress.
Problem toksyczności tlenu i jego wpływu na układ nerwowy jest zagadnieniem ważnym wobec stosowania tlenu i mieszanin oddechowych w praktyce nurkowej., oraz w świetle uderzającego synergizmu działania tlenu i promieniowania jonizującego. Badania poziomu nadtlenków lipidów wykonywano w mózgu szczurów. Zwierzęta poddawano wyczerpującemu wysiłkowi w komorze ciśnieniowej pod działaniem tlenu przy ciśnieniu od 0-3 atn w okresie 2560 minut. Równolegle przeprowadzano badania na zwierzętach znajdujących się w spoczynku. Po wypreparowaniu mózg homogenizowano i oznaczono nadtlenki lipidów metodą Wollmana z TBA. U zwierząt obciążonych wysiłkiem fizycznym w podanych przedziałach czasu, nie stwierdzono odchyleń w poziomie nadtlenków lipidów, w porównaniu z grupą kontrolną. Wzrost poziomu nadtlenków lipidów stwierdzono u szczurów u których wystąpiły objawy zatrucia tlenowego. Na podstawie powyższych wyników autorzy przypuszczają, że wzrost nadtlenków lipidów mózgu w przypadkach hiperbarii tlenowej należy uznać za daleko posunięty szkodliwy efekt działania tlenu, następujący po uszkodzeniu enzymatycznym oraz zachwianiu obrony antyoksydatywnej komórek. Przy niskich nadciśnieniach tlenu nie stwierdzono odchyleń w poziomie nadtlenków lipidów, w porównaniu z grupą kontrolną.
EN
The problem of oxygen toxicity, and its effect on the nervous system, is an important topic with regard to the application of oxygen and breathing mixes in the pursuit of diving, as well as in the light of the striking synergy between the effects of oxygen and ionising radiation. Studies on the level of lipid peroxides were performed on rat brains. The animals were subjected to exhaustive physical strain in a pressure chamber and oxygen at the pressure between 0-3 atm for the period of 25-60 minutes. Parallel research was conducted on rested animals. Following the dissection, the brain was homogenised and the levels of lipid peroxides were determined using the Wollman method with TBA. In animals subjected to physical effort over the specified time, no deviations in the levels of lipid peroxides were observed in comparison to the control group. An increase in lipid peroxide level was noted in rats manifesting oxygen toxicity symptoms. On the basis of the above findings, the authors presume that the growth of lipid peroxides in the brain in cases subjected to hyperbaric oxygenation should be recognised as a far-reaching harmful effect of oxygen, occurring after enzymatic damage and the violation of cellular antioxidant protection. At low oxygen overpressures, no deviations in the levels of lipid peroxides were noted as compared to the control group.
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