scholarly journals High Endurance Elite Athletes Show Age-dependent Lower Levels of Circulating Complements Compared to Low/Moderate Endurance Elite Athletes

2021 ◽  
Vol 8 ◽  
Author(s):  
Shamma Al-Muraikhy ◽  
Manjunath Ramanjaneya ◽  
Alexander S. Dömling ◽  
Ilham Bettahi ◽  
Francesco Donati ◽  
...  

Introduction: Aerobic exercise activates the complement system in the peripheral blood. However, the effect of age and high intensity endurance training on the levels of circulating complements and sassociated inflammatory cytokines, oxidative stress markers and cellular aging remains unknown.Methods: In this study, serum samples from 79 elite athletes who belong to high (n = 48) and low/moderate (n = 31) endurance sports and two age groups (below 30 years old, n = 53, and above 30 years old, n = 26) were profiled for 14 complements. Linear models were used to assess differences in complements levels between sport and age groups. Spearmann’s correlation was used to assess the relationship among detected complements and proinflammatory cytokines, oxidative stress markers and telomere lengths.Results: High endurance elite athletes exhibited significantly lower levels of circulating C2, C3b/iC3b and adipsin complements than their age-matched low/moderate endurance counterparts. Levels of C2, adipsin and C3b/iC3b were positively correlated with most detected complements, the pro-inflammatory cytokines TNF-alpha and IL-22 and the anti-oxidant enzyme catalase. However, they were negatively correlated with telomere length only in younger elite athletes regardless of their sport groups. Furthermore, high endurance elite athletes showed significantly lower concentrations of C3b/iC3b, C4b, C5, C5a, C1q, C3, C4, factor H and properdin in younger athletes compared to their older counterparts.Conclusion: Our novel data suggest that high endurance elite athletes exhibit age-independent lower levels of circulating C2, C3b/iC3b and adipsin, associated with lower inflammatory, oxidative stress and cellular aging, as well as lower levels of 10 other complements in younger athletes compared to older counterparts. Assessing the effect of various levels of endurance sports on complements-based immune response provides a better understanding of exercise physiology and pathophysiology of elite athletes.

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Barbara A. Bażanów ◽  
Elżbieta Chełmecka ◽  
Ewa Romuk ◽  
Dominika M. Stygar

Hucul and Arabian horses differ in the physiological constitution and exposition to environmental conditions. Oxidative stress plays a pathogenic role in many diseases and enables further injuries. The objective of this study was to compare the levels of enzymatic and nonenzymatic oxidative stress markers in Hucul horses living in seminatural conditions and in commercially handled Arabian horses. We tested the serum samples for total superoxide dismutase (total SOD), Cu-Zn-superoxide dismutase (CuZnSOD), and Mn-dependent superoxide dismutase (MnSOD) activity; for lipofuscin (LPS), ceruloplasmin (CER) and malondialdehyde (MDA) concentration; and for total antioxidant capacity (TAC) and total oxidant status (TOS). Total SOD (p<0.001), MnSOD (p<0.001), and CuZnSOD (p<0.001) activities were significantly higher whereas LPS (p<0.05), TAC (p<0.001), TOS (p<0.001), and MDA (p<0.001) concentrations were significantly lower in the serum samples collected from Huculs vs. Arabian horses, regardless of the gender. Gender, regardless of the breed, had no significant impact on the antioxidants’ activity and concentration. Total SOD and MnSOD activities were significantly higher in Hucul’s mares when compared to Hucul’s stallions. Concentrations of TAC and TOS were significantly lower in Arabian stallions than in Arabian mares. Commercially handled horses expressed a higher level of oxidative stress markers in comparison to breeds living in seminatural conditions. We conclude that antioxidants are important biomarkers of animal health, whether they are under maintenance care or performing physical exercise.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Hiroshi Takahashi ◽  
Yasuchika Aoki ◽  
Junya Saito ◽  
Arata Nakajima ◽  
Masato Sonobe ◽  
...  

Recent reports indicate that oxidative stress is involved in the pathobiology of acute spinal cord injury or compression myelopathy. We conducted an observational study to determine levels of oxidative stress markers in serum from 80 patients who underwent spinal surgery to treat neurological symptoms related to lumbar degenerative disorders. Serum samples were collected before surgery and at 3 months, 6 months, and 1 year after surgery. Derivatives of reactive oxygen metabolites (ROM) in the serum samples were measured to gauge the level of oxidative stress. For preoperative neurological evaluation, patients were assessed for motor weakness in the lower extremities. We divided the patient samples into two groups: ROM decreasing at 1 year after surgery (G group) and ROM increasing at 1 year after surgery (W group). Then, we evaluated clinical outcomes using the visual analog scale and Oswestry disability index (ODI). Among the samples from the 80 enrolled patients, mean ROM levels before surgery increased to 388.5 ± 92.0 , indicating the presence of moderate oxidative stress. The level of ROM gradually decreased after surgery and 1 year after surgery: the levels had significantly decreased to 367.6 ± 83.3 ( p < 0.05 ). In patients who exhibited motor weakness, ROM values were significantly increased compared to those patients who had no motor weakness ( p < 0.05 ). In analyses of clinical outcomes, ODI values for the W group 1 year after surgery were significantly higher than those for the G group ( p < 0.05 ). Moderate oxidative stress was present in patients who had lumbar degenerative disorders and the degree of oxidative stress gradually improved within 1 year after surgery. The clinical results suggest that neurogenic oxidative stress can be mitigated by surgery for patients with lumbar degenerative disorders, and residual oxidative stress reflects poor surgical outcomes.


2012 ◽  
Vol 46 (6) ◽  
pp. 819-824 ◽  
Author(s):  
Mariana Pedrini ◽  
Raffael Massuda ◽  
Gabriel R. Fries ◽  
Matheus A. de Bittencourt Pasquali ◽  
Carlos Eduardo Schnorr ◽  
...  

2021 ◽  
Vol 14 (4) ◽  
pp. 380
Author(s):  
Hadeel Alsaegh ◽  
Hala Eweis ◽  
Fatemah Kamal ◽  
Aziza Alrafiah

The risk of developing epilepsy is strongly linked to peripheral inflammatory disorders in humans. High-mobility group box protein 1 (HMGB1) has the most focus for being a suspect in this scenario. The current study aimed to detect the celecoxib effect, an anti-inflammatory drug, on decreasing seizure susceptibility and organ damage in lipopolysaccharides (LPS)/pilocarpine (PILO) pretreated Wistar rats. Rats were divided into 6 groups (8 each): group 1 (control), group 2 (PILO), group 3 (PILO+LPS), group 4 (PILO+LPS+(VPA) Valproic acid), group 5 (PILO+LPS+Celecoxib), and group 6 (PILO+LPS+VPA+Celecoxib). LPS was used to induce sepsis and PILO to induce seizures. Oxidative stress markers, pro-inflammatory cytokines, and HMGB1 levels in serum and brain homogenate were evaluated. Histopathological studies were conducted on the hippocampus, liver, lung, and kidney. Treatment with celecoxib either alone or in combination with VPA significantly reduced Racine score and delays latency to generalized tonic-clonic seizures onset with a significant decrease in hippocampal levels of pro-inflammatory cytokines, oxidative stress markers, and increase in reduced glutathione. In addition, celecoxib treatment either alone or in combination with VPA suppressed HMGB1translocation into peripheral circulation more than treatment with VPA alone. Furthermore, hippocampus, liver, lung, and kidney histopathological changes were improved in contrast to other epileptic groups. Celecoxib either alone or combined with VPA has antiepileptic and multiorgan protective effects on acute seizures and inflammatory models induced by PILO with LPS. It decreased histopathological findings, oxidative, and inflammatory effects induced by VPA and LPS. This might be due to its anti-oxidative, anti-inflammatory and anti-HMGB1 mediated effects.


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Suzan A. Khodir ◽  
Rehab M. Samaka ◽  
Omnia Ameen

Introduction. Not only is diabetic nephropathy (DN) the most common cause of end-stage renal disease worldwide, but it also increases the risk of mortality up to fourteen times compared to normoalbuminuric diabetic patients. Aim. The aim of the current study was the evaluation of the renoprotective effects of vitamin D in DN and the possible interplay between autophagy and mTOR pathways. Materials and Methods. Fifty male Wistar albino rats were divided (10/group) into control, DN group, insulin-treated DN group, vitamin D-treated DN group, and combined insulin and vitamin D-treated DN group. Assessments of systolic blood pressure, albuminuria, creatinine clearance, serum glucose, insulin, urea, creatinine, inflammatory cytokines, oxidative stress markers, and rat kidney gene expression of mTOR were performed. Histopathological and immunohistochemical assessments of autophagy marker LC3 in rat kidneys were also performed. Results. DN was associated with significant increases in SBP, urinary albumin, serum glucose, urea, creatinine, inflammatory cytokines, MDA, and mTOR gene expression (P<0.05). However, there was significant decrease in creatinine clearance, serum insulin, GSH, and H score value of LC3 when compared with control group (P<0.05). The combination of insulin and vitamin D treatment significantly restored DN changes when compared with the other treated groups, except in oxidative stress markers where there was an insignificant difference between the combination-treated and insulin-treated groups (P>0.05). Conclusion. It has been concluded that vitamin D is a potent adjuvant therapy in treatment of DN via downregulation of mTOR gene expression, stimulation of autophagy, and antioxidant, anti-inflammatory, and hypotensive effects.


2019 ◽  
Vol 17 ◽  
pp. 205873921984554
Author(s):  
Zhiming Song ◽  
Paul Weigl ◽  
Bi Wang

This study aimed to analyze the correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases (MMPs) in gingival crevicular fluid (GCF) with peri-implantitis (PI). Forty patients receiving dental implantation were enrolled. There were 52 implants, which were divided into PI group (42 implants) and health implant (HI) group (10 implants). Fifty-two healthy teeth (HT) with the same names with affected teeth in the patients were selected as the control group. The periodontal status was recorded. The GCF was collected and quantified. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), hypersensitive C-reactive protein (hs-CRP), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), MMP-13, and MMP-8 were detected using enzyme-linked immunosorbent assay (ELISA). Results showed that the probing depth, sulcus bleeding index, GCF volume, and TNF-α, IL-6, hs-CRP, MMP-8, and MMP-13 levels in GCF in PI group were significantly higher than HI and HT groups, respectively ( P < 0.01 or P < 0.05). The SOD and GSH-Px levels in PI group were significantly lower than HI and HT groups, respectively ( P < 0.05). Excepting hs-CRP, there was no significant difference of each index between HI and HT groups ( P > 0.05). In conclusion, TNF-α, IL-6, hs-CRP, SOD, GSH-Px, MMP-8, and MMP-13 are involved in the occurrence of PI, and they may be used as auxiliary indicators to evaluate the degree of PI. In addition, the clinical periodontal index probing depth and sulcus bleeding index are positively correlated with GCF volume, hs-CRP, MMP-8, and MMP-13.


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