scholarly journals Biochemical profile in mixed martial arts athletes

PeerJ ◽  
2022 ◽  
Vol 10 ◽  
pp. e12708
Author(s):  
Łukasz Marcin Tota ◽  
Szczepan Stanisław Wiecha
Keyword(s):  
Creatine Kinase ◽  
Uric Acid ◽  
Tumor Necrosis Factor ◽  
Martial Arts ◽  
Tumor Necrosis ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Mixed Martial Arts ◽  
Biochemical Indicators ◽  
Necrosis Factor

The study aimed to evaluate changes in selected biochemical indicators among mixed martial arts competitors in subsequent periods of the training cycle. The research involved 12 mixed martial arts athletes aged 25.8 ± 4.2 years competing in the intermediate category. Selected somatic indicators were measured twice. Biochemical indicators were assessed five times during the 14-week study period. Serum concentrations of testosterone, cortisol, uric acid, myoglobin, total protein, interleukin 6, and tumor necrosis factor, as well as creatine kinase activity were determined. One hour after sparring completion, there were significant increases in cortisol (by 54.9%), uric acid (22.0%), myoglobin (565.0%), and interleukin 6 (280.3%) as compared with the values before the simulated fight. The highest creatine kinase activity (893.83 ± 139.31 U/l), as well as tumor necrosis factor (3.93 ± 0.71 pg/ml) and testosterone (5.83 ± 0.81 ng/ml) concentrations (p = 0.00) were recorded 24 hours after the simulation. Systematic observation of selected blood biochemical indicators in the training process periodization in mixed martial arts helps understand adaptive, compensatory, and regenerative mechanisms occurring in training athletes.

Thiopental Inhibits Tumor Necrosis Factor α–induced Activation of Nuclear Factor κB through Suppression of IκB Kinase Activity

2003 ◽  
Vol 99 (2) ◽  
pp. 360-367 ◽  
Author(s):  
Torsten Loop ◽  
Matjaz Humar ◽  
Soeren Pischke ◽  
Alexander Hoetzel ◽  
Rene Schmidt ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
T Lymphocytes ◽  
Tumor Necrosis ◽  
Kinase Activity ◽  
Inhibitory Effect ◽  
Nuclear Factor ◽  
Ikappab Kinase ◽  
Gaba A ◽  
Nf Kappab ◽  
Necrosis Factor

Background Thiopental is frequently used for the treatment of intracranial hypertension after severe head injury and is associated with immunosuppressive effects. The authors have recently reported that thiopental inhibits activation of nuclear factor (NF) kappaB, a transcription factor implicated in the expression of many inflammatory genes. Thus, it was the aim of the current study to examine the molecular mechanism of this inhibitory effect. Methods The authors tested gamma-aminobutyric acid (GABA), the GABA(A) antagonist bicuculline, and the GABA(B) antagonist dichlorophenyl-methyl-amino-propyl-diethoxymethyl-phosphinic acid (CGP 52432) in combination with thiopental for their influence on the activation of NF-kappaB. In addition, they investigated the direct effect of thiopental on activated NF-kappaB DNA binding activity. These experiments were conducted in Jurkat T lymphocytes using electrophoretic mobility shift assays. The presence of the phosphorylated and dephosphorylated NF-kappaB inhibitor IkappaBalpha (Western blotting) and IkappaB kinase activity were studied in Jurkat T cells and human CD3+ T lymphocytes. In addition, the authors tested the effect of the structural barbiturate analog pairs thiopental-pentobarbital and thiamylal-secobarbital and of thiopental in combination with the thio-group containing chemical dithiothreitol on the activation of NF-kappaB. Results GABA did not inhibit NF-kappaB activation, and the GABA(A) and GABA(B) antagonists bicuculline and CGP did not diminish the thiopental-mediated inhibitory effect on NF-kappaB activation. Thiopental did not inhibit activated NF-kappaB directly in a cell-free system. The phosphorylation of IkappaBalpha was prevented after incubation with 1,000 microg/ml thiopental. The same concentration of thiopental also inhibited IkappaB kinase activity in tumor necrosis factor-stimulated Jurkat T cells and human CD3+ T lymphocytes (60% suppression, P < 0.05 vs. tumor necrosis factor alpha alone). Thiobarbiturates (4 x 10(-3) m) inhibited NF-kappaB activity, whereas equimolar concentrations of the structural oxyanalogs did not. Preincubation of thiopental with dithiothreitol diminished the inhibitory effect. Conclusion Thiopental-mediated inhibition of NF-kappaB activation is due to the suppression of IkappaB kinase activity and depends at least in part on the thio-group of the barbiturate molecule.

scholarly journals Assessment of Lipocalin 2, Clusterin, Soluble Tumor Necrosis Factor Receptor-1, Interleukin-6, Homocysteine, and Uric Acid Levels in Patients with Psoriasis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Arzu Ataseven ◽  
Recep Kesli ◽  
Gulcan Saylam Kurtipek ◽  
Perihan Ozturk
Keyword(s):  
Uric Acid ◽  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Severity Index ◽  
Serum Levels ◽  
Lipocalin 2 ◽  
Pasi Score ◽  
Necrosis Factor

Background. Chronic inflammation may play a role in psoriasis pathogenesis. Lipocalin 2, clusterin, soluble tumor necrosis factor receptor-1 (sTNFR-1), interleukin-6, homocysteine, and uric acid are inflammatory and/or biochemical markers. However, both the roles of these markers and the pathogenesis of psoriasis are unknown.Objective. The aim of this study was to investigate serum levels of lipocalin 2, clusterin, sTNFR-1, interleukin-6, homocysteine, and uric acid in patients and controls groups.Methods. Fifty-six patients with psoriasis and 33 healthy controls were included in the study. Serum concentrations of the markers were evaluated by ELISA. The Psoriasis Area and Severity Index (PASI) was evaluated in all psoriasis patients. Body mass index (BMI) was calculated by dividing weight (kg) by height (m) squared.Results. The serum value of lipocalin and sTNFR-1 were significantly higher in psoriasis patients than in controls (resp.,P<0.001,P<0.05). The others showed no significant differences between psoriasis and the control groups (all of themP>0.05). The mean PASI score in the patient group was8.3±6.5.Conclusions. These findings suggest that lipocalin 2 and sTNFR-1 might play a role in the pathogenesis of psoriasis and can be used as markers of the disease.

scholarly journals IκB Kinase α (IKKα) Regulation of IKKβ Kinase Activity

2000 ◽  
Vol 20 (10) ◽  
pp. 3655-3666 ◽  
Author(s):  
Yumi Yamamoto ◽  
Min-Jean Yin ◽  
Richard B. Gaynor
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Kinase Activity ◽  
Necrosis Factor Alpha ◽  
Iκb Kinase ◽  
Factor Alpha ◽  
Subsequent Activation ◽  
Necrosis Factor

ABSTRACT Two related kinases, IκB kinase α (IKKα) and IKKβ, phosphorylate the IκB proteins, leading to their degradation and the subsequent activation of gene expression by NF-κB. IKKβ has a much higher level of kinase activity for the IκB proteins than does IKKα and is more critical than IKKα in modulating tumor necrosis factor alpha activation of the NF-κB pathway. These results indicate an important role for IKKβ in activating the NF-κB pathway but leave open the question of the role of IKKα in regulating this pathway. In the current study, we demonstrate that IKKα directly phosphorylates IKKβ. Moreover, IKKα either directly or indirectly enhances IKKβ kinase activity for IκBα. Finally, transfection studies to analyze NF-κB-directed gene expression suggest that IKKα is upstream of IKKβ in activating the NF-κB pathway. These results indicate that IKKα, in addition to its previously described ability to phosphorylate IκBα, can increase the ability of IKKβ to phosphorylate IκBα.

scholarly journals Transient IκB Kinase Activity Mediates Temporal NF-κB Dynamics in Response to a Wide Range of Tumor Necrosis Factor-α Doses

2005 ◽  
Vol 281 (5) ◽  
pp. 2945-2950 ◽  
Author(s):  
Raymond Cheong ◽  
Adriel Bergmann ◽  
Shannon L. Werner ◽  
Joshua Regal ◽  
Alexander Hoffmann ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Kinase Activity ◽  
Iκb Kinase ◽  
Wide Range ◽  
Factor Α ◽  
Necrosis Factor
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