scholarly journals Fermented Oyster Extract Attenuated Dexamethasone-Induced Muscle Atrophy by Decreasing Oxidative Stress

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7128
Author(s):  
Seyeon Oh ◽  
Chang Hu Choi ◽  
Bae-Jin Lee ◽  
Joung-Hyun Park ◽  
Kuk-Hui Son ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Grip Strength ◽  
Muscle Atrophy ◽  
Ubiquitin Ligase ◽  
Aminobutyric Acid ◽  
Sod Activity ◽  
Cross Sectional ◽  
Attenuation Effect ◽  
Tnf Α ◽  
Antioxidative Effects

It is well known that oxidative stress induces muscle atrophy, which decreases with the activation of Nrf2/HO-1. Fermented oyster extracts (FO), rich in γ-aminobutyric acid (GABA) and lactate, have shown antioxidative effects. We evaluated whether FO decreased oxidative stress by upregulating Nrf2/HO-1 and whether it decreased NF-κB, leading to decreased IL-6 and TNF-α. Decreased oxidative stress led to the downregulation of Cbl-b ubiquitin ligase, which increased IGF-1 and decreased FoxO3, atrogin1, and Murf1, and eventually decreased muscle atrophy in dexamethasone (Dexa)-induced muscle atrophy animal model. For four weeks, mice were orally administered with FO, GABA, lactate, or GABA+Lactate, and then Dexa was subcutaneously injected for ten days. During Dexa injection period, FO, GABA, lactate, or GABA+Lactate were also administered, and grip strength test and muscle harvesting were performed on the day of the last Dexa injection. We compared the attenuation effect of FO with GABA, lactate, and GABA+lactate treatment. Nrf2 and HO-1 expressions were increased by Dexa but decreased by FO; SOD activity and glutathione levels were decreased by Dexa but increased by FO; NADPH oxidase activity was increased by Dexa but decreased by FO; NF-κB, IL-6, and TNF-α activities were increased by Dexa were decreased by FO; Cbl-b expression was increased by Dexa but restored by FO; IGF-1 expression was decreased by Dexa but increased by FO; FoxO3, Atrogin-1, and MuRF1 expressions were increased by Dexa but decreased by FO. The gastrocnemius thickness and weight were decreased by Dexa but increased by FO. The cross-sectional area of muscle fiber and grip strength were decreased by Dexa but increased by FO. In conclusion, FO decreased Dexa-induced oxidative stress through the upregulation of Nrf2/HO-1. Decreased oxidative stress led to decreased Cbl-b, FoxO3, atrogin1, and MuRF1, which attenuated muscle atrophy.

scholarly journals IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions

2016 ◽  
Vol 38 (6) ◽  
pp. 2163-2172 ◽  
Author(s):  
Xiaorong Hu ◽  
Ruisong Ma ◽  
Jiajia Lu ◽  
Kai Zhang ◽  
Weipan Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Tunel Staining ◽  
Ischemia And Reperfusion ◽  
Stress Reactions ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Tnf Α ◽  
And Oxidative Stress

Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group. At 4 h after reperfusion, the serum concentration of lactate dehydrogenase (LDH), creatine kinase (CK) and the tissue MDA concentration and SOD activity were measured. The infarcte size was measured by TTC staining. Apoptosis in heart sections were measured by TUNEL staining. The expression of HMGB1 and IL-17A were detected by Western Blotting and the expression of TNF-α and IL-6 were detected by Elisa. Results: After 4 h reperfusion, compared with the I/R group, IL-23 significantly increased the infarct size, the apoptosis of cardiomyocytes and the levels of LDH and CK (all P < 0.05). Meanwhile, IL-23 significantly increased the expression of eIL-17A, TNF-α and IL-6 and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R (all P<0.05). IL-23 had no effect on the expression of HMGB1 (p > 0.05). All these effects were abolished by anti-IL-23 administration. Conclusion: The present study suggested that IL-23 may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

scholarly journals TNFα Mediates the Interaction of Telomeres and Mitochondria Induced by Hyperglycemia: A Rural Community-Based Cross-Sectional Study

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Lu Lyu ◽  
Shuli He ◽  
Huabing Zhang ◽  
Wei Li ◽  
Jingbo Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glucose Tolerance ◽  
Rural Community ◽  
Rural China ◽  
Inflammatory Factors ◽  
Oral Glucose ◽  
Sod Activity ◽  
Cross Sectional ◽  
Mitochondrial Dna Copy Number ◽  
The Relationship

This study is aimed at evaluating the relationship between leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNAcn) in a noninterventional rural community of China with different glucose tolerance statuses. In addition, we investigate whether the indicators of oxidative stress and inflammation were involved and identify mediators among them. A total of 450 subjects in rural China were included and divided into two groups according to a 75 g oral glucose tolerance test (OGTT): the abnormal glucose metabolism (AGM, n=257, 57.1%) group and the normal glucose tolerance (NGT, n=193, 42.9%) group. Indicators of oxidative stress (superoxide dismutase (SOD) and glutathione reductase (GR)) and inflammatory indices (tumor necrosis factor α (TNFα) and interleukin-6 (IL-6)) were all determined by ELISA. LTL and mtDNAcn were measured using a real-time PCR assay. Linear regressions were used to adjust for covariates that might affect the relationship between LTL and mtDNAcn. Mediation analyses were utilized to evaluate the mediators. In the AGM, LTL was correlated with mtDNAcn (r=0.214, p=0.001), but no correlation was found in the NGT. The association between LTL and mtDNAcn was weakened after adjusting for inflammatory factors in the AGM (p=0.087). LTL and mtDNAcn were both inversely related to HbA1c, IL-6, TNFα, and SOD activity. Mediation analysis demonstrated that TNFα was a significant mediator in the telomere-mitochondrial interactome in the AGM. This result suggests that inflammation and oxidative stress may play a vital role in telomere shortening as well as mitochondrial dysfunction. In the subjects with hyperglycemia, a significant positive correlation is observed between LTL and mtDNAcn, which is probably mediated by TNFα. TNFα may be considered a potential therapeutic target against aging-related disease in hyperglycemia.

scholarly journals The effect of long-term dehydration and subsequent rehydration on markers of inflammation, oxidative stress and apoptosis in the camel kidney

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Mahmoud A. Ali ◽  
Hassan Abu Damir ◽  
Osman M. Ali ◽  
Naheed Amir ◽  
Saeed Tariq ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Water Conservation ◽  
Mesangial Cells ◽  
Expression Level ◽  
Kidney Cortex ◽  
Mrna Levels ◽  
Sod Activity ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Different Response

Abstract Background Dehydration has deleterious effects in many species, but camels tolerate long periods of water deprivation without serious health compromise. The kidney plays crucial role in water conservation, however, some reports point to elevated kidney function tests in dehydrated camels. In this work, we investigated the effects of dehydration and rehydration on kidney cortex and medulla with respect to pro-inflammatory markers, oxidative stress and apoptosis along with corresponding gene expression. Results The cytokines IL-1β and IL-18 levels were significantly elevated in the kidney cortex of dehydrated camel, possibly expressed by tubular epithelium, podocytes and/or mesangial cells. Elevation of IL-18 persisted after rehydration. Dehydration induced oxidative stress in kidney cortex evident by significant increases in MDA and GSH, but significant decreases in SOD and CAT. In the medulla, CAT decreased significantly, but MDA, GSH and SOD levels were not affected. Rehydration abolished the oxidative stress. In parallel with the increased levels of MDA, we observed increased levels of PTGS1 mRNA, in MDA synthesis pathway. GCLC mRNA expression level, involved in GSH synthesis, was upregulated in kidney cortex by rehydration. However, both SOD1 and SOD3 mRNA levels dropped, in parallel with SOD activity, in the cortex by dehydration. There were significant increases in caspases 3 and 9, p53 and PARP1, indicating apoptosis was triggered by intrinsic pathway. Expression of BCL2l1 mRNA levels, encoding for BCL-xL, was down regulated by dehydration in cortex. CASP3 expression level increased significantly in medulla by dehydration and continued after rehydration whereas TP53 expression increased in cortex by rehydration. Changes in caspase 8 and TNF-α were negligible to instigate extrinsic apoptotic trail. Generally, apoptotic markers were extremely variable after rehydration indicating that animals did not fully recover within three days. Conclusions Dehydration causes oxidative stress in kidney cortex and apoptosis in cortex and medulla. Kidney cortex and medulla were not homogeneous in all parameters investigated indicating different response to dehydration/rehydration. Some changes in tested parameters directly correlate with alteration in steady-state mRNA levels.

scholarly journals Effect of Forced Physical Activity on the Severity of Experimental Colitis in Normal Weight and Obese Mice. Involvement of Oxidative Stress and Proinflammatory Biomarkers

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1127 ◽  
Author(s):  
Jan Bilski ◽  
Agnieszka Mazur-Bialy ◽  
Dagmara Wojcik ◽  
Marcin Magierowski ◽  
Marcin Surmiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treadmill Exercise ◽  
Experimental Colitis ◽  
Treadmill Running ◽  
Adaptation Period ◽  
Obese Mice ◽  
Trinitrobenzenesulfonic Acid ◽  
Sod Activity ◽  
Tnf Α ◽  
Colonic Blood Flow

Inflammatory bowel diseases are a heterogeneous group of disorders represented by two major phenotypic forms, Crohn’s disease and ulcerative colitis. Cross talk between adipokines and myokines, as well as changes in intestinal microcirculation, was proposed in pathogenesis of these disorders. C57BL/6 male mice were fed ad libitum for 12 weeks a standard (SD) or high-fat diet (HFD). After the adaptation period, two groups of animals fed SD or HFD were subjected to 6 weeks of the forced treadmill exercise and the experimental colitis was induced in both groups of sedentary and exercising mice fed SD and HFD by intra-colonic administration of 2,4,6-trinitrobenzenesulfonic acid. The disease activity index (DAI), colonic blood flow (CBF), the weight of animals, caloric intake, the mesenteric fad pad, the colonic oxidative stress markers malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) activity and intestinal expression and protein content of proinflammatory markers were evaluated. Macroscopic and microscopic colitis in sedentary SD mice was accompanied by a significant fall in CBF and exacerbated in those fed a HFD. The contents of MDA, GSH, and SOD activity were significantly increased in both SD and HFD fed mice with treadmill exercise as compared with sedentary mice. In sedentary HFD mice a significant increase in the intestinal oxidative stress parameters and mucosal expression of IL-1β, TNF-α, IL-17, IFNγ, IL-6, and IL-10 protein were observed and these effects were aggravated in mice subjected to forced treadmill exercise. The mucosal expression of mRNA for TNF-α, IL-1β, iNOS, COX-2, SOD-1, SOD-2, GPx mRNAs, and the hypoxia inducible factor (HIF)-1α protein expression were upregulated in colonic mucosa of treadmill exercising HFD mice with colitis compared with those without exercise. We conclude that forced treadmill running exacerbates the severity of colonic damage in obese mice due to a fall in colonic microcirculation, an increase in oxidative stress, and the rise in expression and activity of proinflammatory biomarkers.

scholarly journals Effects of <i>γ</i>-aminobutyric acid on the tissue structure, antioxidant activity, cell apoptosis, and cytokine contents of bursa of Fabricius in chicks under heat stress

2016 ◽  
Vol 59 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Zhong Chen ◽  
Yong-Wei Zhou ◽  
Chen Liang ◽  
Ying-Ya Jiang ◽  
Li-Jin Xie
Keyword(s):  
Antioxidant Activity ◽  
Heat Stress ◽  
Cell Apoptosis ◽  
Aminobutyric Acid ◽  
Bursa Of Fabricius ◽  
Tissue Structure ◽  
Regulation Mechanism ◽  
Sod Activity ◽  
Tnf Α ◽  
Significant Difference

Abstract. This study aims to investigate the changes in the tissue structure, cell apoptosis, antioxidant activity, and cytokine contents of the bursa of Fabricius (BF) in chicks under heat stress, and the regulation mechanism of the protective effect of dietary γ-aminobutyric acid (GABA) on BF in chicks. One-day-old male Wenchang chicks were randomly divided into a control group (CK), heat stress group (HS), and GABA + HS group. The index of BF, area of follicle, density of apoptosis, antioxidant activity (SOD, MDA, and GSH-PX), and cytokine contents (IL-1β, IL-6, TNF-α, and HSP70) in the BF tissue of chicks were determined at the end of week 1–6. Results showed that HS group had significantly decreased index of BF and area of follicle, and significantly increased density of apoptosis compared with CK group (P < 0.05), while GABA + HS group had significantly increased index of BF and area of follicle, and significantly decreased density of apoptosis compared with HS group (P < 0.05). There was no significant difference in the total SOD activity in the BF tissue among the three groups, except that GABA + HS group had an increase in total SOD activity in week 6, which was significantly different from that of CK and HS groups (P < 0.05). The GSH-PX activity in the BF tissue was high in all groups in the first 3 weeks, but decreased in week 4–6. The MDA content in the BF tissue of HS and GABA + HS groups was significantly increased compared with that of CK group (P < 0.05). There was no significant difference in the HSP70 content between HS and GABA + HS groups (P > 0.05), both of which were significantly decreased compared with that of CK group (P < 0.05). The contents of IL-1β, IL-6, and TNF-α in the BF tissue increased with age in all three groups in week 1–6. In the later BF development, the content of IL-1β in HS group was significantly decreased compared with that of CK group, whereas the content of IL-6 was significantly increased (P < 0.05), and no significant difference was observed in the content of TNF-α. In contrast, the content of IL-6 in GABA + HS group was significantly decreased compared with that of CK group, and the content of TNF-α was significantly increased (P < 0.05). These results suggested that heat stress caused structural damage to the BF tissue, increased cell apoptosis, and decreased antioxidant activity in the BF of chicks. GABA could alleviate the negative effects of heat stress on the BF tissue and improve the structural and functional development of BF in chicks, by increasing the antioxidant activity, down-regulating IL-6 content, and reducing cell apoptosis in the BF tissue of chicks.

scholarly journals Soy Glycinin Contains a Functional Inhibitory Sequence against Muscle-Atrophy-Associated Ubiquitin Ligase Cbl-b

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Tomoki Abe ◽  
Shohei Kohno ◽  
Tomonari Yama ◽  
Arisa Ochi ◽  
Takuro Suto ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Ubiquitin Ligase ◽  
Soy Protein ◽  
Tibialis Anterior Muscle ◽  
Soy Protein Isolate ◽  
Protein Isolate ◽  
Skeletal Muscle Atrophy ◽  
Cross Sectional ◽  
Wet Weight ◽  
The Right

Background. Unloading stress induces skeletal muscle atrophy. We have reported that Cbl-b ubiquitin ligase is a master regulator of unloading-associated muscle atrophy. The present study was designed to elucidate whether dietary soy glycinin protein prevents denervation-mediated muscle atrophy, based on the presence of inhibitory peptides against Cbl-b ubiquitin ligase in soy glycinin protein.Methods. Mice were fed either 20% casein diet, 20% soy protein isolate diet, 10% glycinin diet containing 10% casein, or 20% glycinin diet. One week later, the right sciatic nerve was cut. The wet weight, cross sectional area (CSA), IGF-1 signaling, and atrogene expression in hindlimb muscles were examined at 1, 3, 3.5, or 4 days after denervation.Results. 20% soy glycinin diet significantly prevented denervation-induced decreases in muscle wet weight and myofiber CSA. Furthermore, dietary soy protein inhibited denervation-induced ubiquitination and degradation of IRS-1 in tibialis anterior muscle. Dietary soy glycinin partially suppressed the denervation-mediated expression of atrogenes, such as MAFbx/atrogin-1 and MuRF-1, through the protection of IGF-1 signaling estimated by phosphorylation of Akt-1.Conclusions. Soy glycinin contains a functional inhibitory sequence against muscle-atrophy-associated ubiquitin ligase Cbl-b. Dietary soy glycinin protein significantly prevented muscle atrophy after denervation in mice.

Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion

2006 ◽  
Vol 291 (6) ◽  
pp. R1756-R1763 ◽  
Author(s):  
John M. Lawler ◽  
Hyo-Bum Kwak ◽  
Wook Song ◽  
Janet L. Parker
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Stress Proteins ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Sod Activity ◽  
Tnf Α

Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-α, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups ( n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-α and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (−45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher ( P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.

scholarly journals A transient antioxidant stress response accompanies the onset of disuse atrophy in human skeletal muscle

2009 ◽  
Vol 107 (2) ◽  
pp. 549-557 ◽  
Author(s):  
Luciano Dalla Libera ◽  
Barbara Ravara ◽  
Valerio Gobbo ◽  
Elena Tarricone ◽  
Maurizio Vitadello ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Stress Response ◽  
Muscle Atrophy ◽  
Cross Sectional Area ◽  
Heme Oxygenase 1 ◽  
Sectional Area ◽  
Cross Sectional ◽  
Protein Levels ◽  
Antioxidant Stress

It is presently unknown whether oxidative stress increases in disused skeletal muscle in humans. Markers of oxidative stress were investigated in biopsies from the vastus lateralis muscle, collected from healthy subjects before [ time 0 (T0)], after 1 wk (T8), and after 5 wk (T35) of bed rest. An 18% decrease in fiber cross-sectional area was detected in T35 biopsies ( P < 0.05). Carbonylation of muscle proteins significantly increased about twofold at T35 ( P < 0.02) and correlated positively with the decrease in fiber cross-sectional area ( P = 0.04). Conversely, T8 biopsies showed a significant increase in protein levels of heme oxygenase-1 and glucose-regulated protein-75 (Grp75)/mitochondrial heat shock protein-70, two stress proteins involved in the antioxidant defense ( P < 0.05). Heme oxygenase-1 increase, which involved a larger proportion of slow fibers compared with T0, appeared blunted in T35 biopsies. Grp75 protein level increased threefold in T8 biopsies and localized especially in slow fibers ( P < 0.025), to decrease significantly in T35 biopsies ( P < 0.05). Percent change in Grp75 levels positively correlated with fiber cross-sectional area ( P = 0.01). Parallel investigations on rat soleus muscles, performed after 1–15 days of hindlimb suspension, showed that Grp75 protein levels significantly increased after 24 h of unloading ( P = 0.02), i.e., before statistically significant evidence of muscle atrophy, to decrease thereafter in relation to the degree of muscle atrophy ( P = 0.03). Therefore, in humans as in rodents, disuse muscle atrophy is characterized by increased protein carbonylation and by the blunting of the antioxidant stress response evoked by disuse.

scholarly journals Role of the angiotensin II AT2 receptor in inflammation and oxidative stress: opposing effects in lean and obese Zucker rats

2011 ◽  
Vol 300 (3) ◽  
pp. F700-F706 ◽  
Author(s):  
Rifat Sabuhi ◽  
Quaisar Ali ◽  
Mohammad Asghar ◽  
Najah Riesh Hadi Al-Zamily ◽  
Tahir Hussain
Keyword(s):  
Oxidative Stress ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Sod Activity ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
And Oxidative Stress

Inflammation and oxidative stress are believed to contribute to hypertension in obesity/diabetes. Recently, we reported a role for the AT2 receptor in blood pressure control in obese Zucker rats. However, the role of AT2 receptors in inflammation and oxidative stress in obesity is not known. Therefore, in the present study, we tested the effects of the AT2 receptor agonist CGP-42112A on inflammation and oxidative stress in obese Zucker rats and compared them in their lean counterparts. Rats were systemically treated with either vehicle (control) or CGP-42112A (1 μg·kg−1·min−1; osmotic pump) for 2 wk. Markers of inflammation (CRP, MCP-1, TNF-α, and IL-6) and oxidative stress (HO-1, gp-91phox) as well as an antioxidant (SOD) were determined. Control obese rats had higher plasma levels of CRP, MCP-1, TNF-α, IL-6, and HO-1 compared with control lean rats. Conversely, plasma SOD activity was lower in control obese than in control lean rats. Furthermore, the protein levels of TNF-α and gp-91phox were higher in the kidney cortex of control obese rats. Interestingly, CGP-42112A treatment in obese rats reduced the plasma and kidney cortex inflammatory (TNF-α, IL-6) and oxidative stress (gp-91phox) markers and increased plasma SOD activity to the levels seen in lean control rats. However, CGP-42112A treatment in lean rats increased inflammatory (TNF-α, IL-6) and oxidative stress (gp-91phox) markers in the plasma and kidney cortex. Our present studies suggest anti-inflammatory and antioxidative functions of AT2 receptor in obese Zucker rats but proinflammatory and prooxidative functions in lean Zucker rats.

scholarly journals DAN MYELOPEROxIDASE) DAN DISFUNGSI ENDOTEL (ASIMETRIK DIMETILARGININ) DI KEGEMUKAN (OBESITAS)

2018 ◽  
Vol 16 (3) ◽  
pp. 128
Author(s):  
Joko Widodo ◽  
Burhanuddin Bahar ◽  
Mansyur Arif
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Central Obesity ◽  
Activity Concentration ◽  
Pathological Condition ◽  
Cross Sectional Study ◽  
Elevated Concentration ◽  
Sod Activity ◽  
Cross Sectional ◽  
Male Subjects

Obesity is a pathological condition in which there is an excess body fat due to imbalance energy expenditure. Its association with oxidative stress could cause other metabolic disorders such as endothelial dysfunction, atherosclerosis, and cardiovascular disease. Theaim of this study was to assess the correlation of oxidative stress (F2-Isoprostane, Superoxide dismutase and Myeloperoxidase) andendothelial dysfunction (Asymmetric dimethylarginine) which happened in central obese men. A cross sectional study was carried outin 62 central obesity male subjects with ages range between 30−60 years. The researcher determined SOD activity, concentration ofMPO as well as ADMA. In this study was found a significant correlation of F2-Isoprostan (r = 0.333, p = 0.008), MPO (r = 0.386; p = 0.008) and ADMA but not with SOD. The elevated concentration of F2-Isoprostane occur 3.5 times (p = 0.02; 95%; CI = 1.19–10.19), elevated MPO occur 3.7 times (p = 0.023; 95%; CI = 1.16–11.56) while combination of elevated F2-Isoprostane-MPO occur6.7 times (p = 0.011; 95%; CI = 1.33-33.24) will increase the risk of endothelial dysfunction. There was a significant correlation of oxidative stress with endothelial dysfunction, and the increase concentration of F2-Isoprostane and MPO indicates the occurrence of endothelial dysfunction in central obesity.

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