Oxidative Stress In Metabolic Syndrome Research Articles

Inhibition of 5-alpha reductase attenuates cardiac oxidative damage in obese and aging male rats via the enhancement of antioxidants and the p53 protein suppression

In aging and metabolic syndrome oxidative stress is a causative factor in the cardiovascular pathology. Upregulation of 5-⍺ reductase is associated with cardiac hypertrophy but how inhibition of 5-⍺ reductase affects cardiometabolic function during oxidative damage under those conditions is unclear. Our hypothesis was that Finasteride (Fin), a 5-⍺ reductase inhibitor, promotes an antioxidant response, leading to an improvement in cardiac function in obese and aging rats. Male rats were divided into 3 groups including normal diet (ND) fed rats, ND-fed rats treated with d-galactose (D-gal) to induce aging, and high-fat diet (HFD) fed rats to induce obesity. Rats received their assigned diet or D-gal for 18 weeks. At week 13, rats in each group were divided into 2 subgroups and received either a vehicle or Fin (5 mg/kg/day, oral gavage). Cardiometabolic and molecular parameters were subsequently investigated. Both D-gal and HFD successfully induced cardiometabolic dysfunction, oxidative stress, mitochondrial dysfunction, and DNA fragmentation. Fin treatment did not affect metabolic disturbances; however, it reduced cardiac sympathovagal imbalance, cardiac dysfunction through the inhibition of oxidative stress and promoted antioxidants, resulting in reduced p53 protein levels and DNA fragmentation. Surprisingly, Fin induced insulin resistance in ND-fed rats. Fin effectively improved cardiac function in both models by enhancing antioxidant levels, suppressing oxidative stress and DNA fragmentation. However, Fin treatment did not confer any beneficial effects on metabolic status. Fin administration effectively improved cardiac sympathovagal balance and cardiac function in rats with oxidative damage induced by either D-gal or HFD.

Association between Nfr2, HO-1, NF-kB Expression, Plasma ADMA, and Oxidative Stress in Metabolic Syndrome.

Endothelial dysfunction is one of the major factors in the pathogenesis of metabolic syndrome (MetS), and its molecular mechanisms are not completely understood. The present study aimed to examine the connection between nuclear factor2-related factor2 (Nrf2), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), heme oxygenase 1 (HO-1), and plasma asymmetric dimethylarginine (ADMA) and malondialdehyde (MDA) in people with MetS. Participants in the study were as follows: with MetS (n = 30) and without MetS (Control) (n = 14). Expression of Nrf2, NF-kB, and HO-1 was measured in peripheral blood mononuclear cells (PBMCs). Plasma ADMA was determined using the ELISA technique and MDA via the thiobarbituric acid method. Our study showed that mRNA of NF-kB, Nrf2, and HO-1 levels in PBMCs in the MetS group were significantly higher than in the controls by 53%, 130%, and 185% (p < 0.05), respectively. Similarly, elevated levels of MDA (by 78%, p < 0.001) and ADMA (by 18.7%, p < 0.001) were established in the MetS group. Our findings show the importance of transcription factor Nrf2, playing an integral role in the protection of the endothelium, and of NF-κB, a transcription factor mediating the inflammatory response in MetS. Knowledge of complex cellular-molecular mechanisms would allow the use of biomarkers such as Nrf2, NF-kB, HO-1, and ADMA for the assessment of endothelial dysfunction in clinical practice.

Mechanisms of Oxidative Stress in Metabolic Syndrome.

Metabolic syndrome is a cluster of conditions associated with the risk of diabetes mellitus type 2 and cardiovascular diseases (CVDs). Metabolic syndrome is closely related to obesity. Increased adiposity promotes inflammation and oxidative stress, which are precursors of various complications involving metabolic syndrome components, namely insulin resistance, hypertension, and hyperlipidemia. An increasing number of studies confirm the importance of oxidative stress and chronic inflammation in the etiology of metabolic syndrome. However, few studies have reviewed the mechanisms underlying the role of oxidative stress in contributing to metabolic syndrome. In this review, we highlight mechanisms by which reactive oxygen species (ROS) increase mitochondrial dysfunction, protein damage, lipid peroxidation, and impair antioxidant function in metabolic syndrome. Biomarkers of oxidative stress can be used in disease diagnosis and evaluation of severity.

An Overview of the TRP-Oxidative Stress Axis in Metabolic Syndrome: Insights for Novel Therapeutic Approaches.

Metabolic syndrome (MS) is a complex pathology characterized by visceral adiposity, insulin resistance, arterial hypertension, and dyslipidaemia. It has become a global epidemic associated with increased consumption of high-calorie, low-fibre food and sedentary habits. Some of its underlying mechanisms have been identified, with hypoadiponectinemia, inflammation and oxidative stress as important factors for MS establishment and progression. Alterations in adipokine levels may favour glucotoxicity and lipotoxicity which, in turn, contribute to inflammation and cellular stress responses within the adipose, pancreatic and liver tissues, in addition to hepatic steatosis. The multiple mechanisms of MS make its clinical management difficult, involving both non-pharmacological and pharmacological interventions. Transient receptor potential (TRP) channels are non-selective calcium channels involved in a plethora of physiological events, including energy balance, inflammation and oxidative stress. Evidence from animal models of disease has contributed to identify their specific contributions to MS and may help to tailor clinical trials for the disease. In this context, the oxidative stress sensors TRPV1, TRPA1 and TRPC5, play major roles in regulating inflammatory responses, thermogenesis and energy expenditure. Here, the interplay between these TRP channels and oxidative stress in MS is discussed in the light of novel therapies to treat this syndrome.

Effects of bariatric surgery versus pharmacological treatment on oxidative stress in metabolic syndrome

Effects of bariatric surgery versus pharmacological treatment on oxidative stress in metabolic syndrome

Markers of Oxidative Stress in Metabolic Syndrome and Antioxidants as an Add-on Therapy in the Reversal of Changes

Markers of Oxidative Stress in Metabolic Syndrome and Antioxidants as an Add-on Therapy in the Reversal of Changes

Effects of purslane supplementation on C-reactive protein levels and biomarkers of oxidative stress as marks for metabolic syndrome: A systematic review and meta-analysis of randomized controlled trials.

The antioxidant and antiinflammatory properties of purslane (Portulaca oleracea L.) are known in preclinical studies but further examination is needed to expand their potential into the clinical scenario. A systematic review and meta-analysis of randomized controlled trials were performed to elucidate the effects of purslane supplementation on C-reactive protein (CRP) levels and biomarkers of oxidative stress in metabolic syndrome, its related complications, and other diseases. PubMed/MEDLINE, Web of Science, SCOPUS, and Embase were the databases searched. Heterogeneity was examined using the I-squared (I2 ) statistic, in which the source of heterogeneity was determined if the I2 -value was >50%. After all the screening processes, 10 studies met the eligibility criteria and were analyzed. Following purslane supplementation, CRP levels decreased significantly (weighted mean difference [WMD]: -0.33 mg/dl, 95% confidence interval [CI]: -0.66, -0.004, p= .047) but with significant heterogeneity (I2 = 87.4%, p= .001). Purslane supplementation did not significantly change serum levels of malondialdehyde (MDA) (WMD: -0.353 μm/L; 95% CI: -0.920, 0.213; I2 = 50.7%), total antioxidant capacity (TAC) (WMD: 0.090 mm/L, 95% CI: -0.081, 0.262; I2 = 47.1%), and superoxide dismutase (SOD) (WMD: 6.54 U/ml, 95% CI: -22.150, 35.236; I2 = 70.7%). Thus, this meta-analysis showed a positive effect of purslane supplementation as a tool to decrease CRP levels, but not to MDA, TAC, and SOD levels.

Dietary Fresh and Boiled Mangkokan Leaves (Nothopanax Scutellarius) Normalized Body Weight, Serum Lipid Profile and Malondialdehyde in Metabolic Syndrome Rats

The antioxidant activity of Nothopanax scutellarius (Burm. f.) Merr, an edible plant, can prevent oxidative stress in metabolic syndrome (MetS). Thus, our research aimed to study the effect of dietary inclusion of fresh or boiled N. scutellarius on body weight and biochemical markers of Wistar rats with MetS. Twenty-four male Wistar rats were divided randomly into four groups, i.e., normal control group, high-fat-high-fructose diet (HFFD) group, fresh N. scutellarius (FNs) group, and boiled N. scutellarius (BNs) group. The normal control group was fed only a standard diet during the entire experiment. High-fat and high-fructose (HFHFr) diet accompanied with 20% fructose in drinking water to induce MetS was given to the HFFD, FNs, and BNs groups for 29 days. This was followed by a 29-day intervention diet in which standard normal diet, fresh N. scutellarius-containing standard diet, and boiled N. scutellarius-containing standard diet were given to the HFFD, FNs, and BNs groups, respectively. HFHFr diet significantly (p&lt;0.05) raised fasting blood glucose (FBG), serum triglyceride, total cholesterol, LDL-cholesterol, and malondialdehyde (MDA), and significantly (p&lt;0.05) reduced HDL-cholesterol. After 29 days on the intervention diet, serum triglycerides, total cholesterol, and LDL-cholesterol levels were found to decrease, and HDL-cholesterol levels were found to increase significantly (p&lt;0.05). Thus, it can be concluded that dietary intake of N. scutellarius for 29 days can improve MetS components, i.e., FBG, serum lipid profile, and MDA, similar to those seen in rats on a normal control diet.

Ossabaw Pig Demonstrates Detrusor Fibrosis and Detrusor Underactivity Associated with Oxidative Stress in Metabolic Syndrome.

Metabolic Syndrome (MetS) has detrimental effects on the bladder, including detrusor underactivity. The progression and mechanism of disease are poorly understood. A swine model for diabetic bladder dysfunction (DBD) was established because of the pig's human-sized bladder and its ability to develop MetS by dietary modification alone. The hypothesis of this study is that this swine model will demonstrate oxidative stress associated with MetS, which contributes to both bladder fibrosis and detrusor underactivity (DU). Ossabaw pigs underwent dietary modification consisting of a hypercaloric, atherogenic diet for 10 mo to induce MetS, and were compared with a group of control (lean) pigs. Urodynamic studies were performed in both groups to confirm DU. Thiobarbituric acid reactive substances (TBARS) detected in the urine were used to measure oxidative stress activity in the urinary tract, and urinary IL17a was used to detect profibrotic activity. MetS was confirmed by assessing body weight, blood pressure, glucose tolerance, total cholesterol, and triglycerides. The MetS group exhibited an increase in the relative levels of urinary TBARS and IL17a. Bladder pressures at capacity were lower in the MetS group, suggesting DU. Histologic analysis of a cohort of control (lean) and MetS pigs revealed that as compared with the control pigs, the MetS pigs had significantly more collagen in the muscularis layer, but not in the submucosa or mucosa layer. In conclusion, the Ossabaw pig model for diet-induced MetS is associated with oxidative stress and profibrotic activity in the bladder, which results in DU. This has previously been shown in mice and rats, but never in pigs. This novel model will better represent human MetS and DBD because the mechanism and size of the pig bladder more closely resemble that of a human, resulting in a more valid model and facilitating further study into the signaling mechanisms responsible for this impairment.

Oxidative Stress and Inflammatory Modulation of Ca2+ Handling in Metabolic HFpEF-Related Left Atrial Cardiomyopathy.

Metabolic syndrome-mediated heart failure with preserved ejection fraction (HFpEF) is commonly accompanied by left atrial (LA) cardiomyopathy, significantly affecting morbidity and mortality. We evaluate the role of reactive oxygen species (ROS) and intrinsic inflammation (TNF-α, IL-10) related to dysfunctional Ca2+ homeostasis of LA cardiomyocytes in a rat model of metabolic HFpEF. ZFS-1 obese rats showed features of HFpEF and atrial cardiomyopathy in vivo: increased left ventricular (LV) mass, E/e’ and LA size and preserved LV ejection fraction. In vitro, LA cardiomyocytes exhibited more mitochondrial-fission (MitoTracker) and ROS-production (H2DCF). In wildtype (WT), pro-inflammatory TNF-α impaired cellular Ca2+ homeostasis, while anti-inflammatory IL-10 had no notable effect (confocal microscopy; Fluo-4). In HFpEF, TNF-α had no effect on Ca2+ homeostasis associated with decreased TNF-α receptor expression (western blot). In addition, IL-10 substantially improved Ca2+ release and reuptake, while IL-10 receptor-1 expression was unaltered. Oxidative stress in metabolic syndrome mediated LA cardiomyopathy was increased and anti-inflammatory treatment positively affected dysfunctional Ca2+ homeostasis. Our data indicates, that patients with HFpEF-related LA dysfunction might profit from IL-10 targeted therapy, which should be further explored in preclinical trials.

The effects of zinc supplementation on metabolic profile and oxidative stress in overweight/obese patients with non-alcoholic fatty liver disease: A randomized, double-blind, placebo-controlled trial

BackgroundEvidence indicates the positive effects of zinc on insulin resistance and oxidative stress in metabolic syndrome or diabetes. Non-alcoholic fatty liver disease (NAFLD) is the main hepatic manifestation of insulin resistance and metabolic syndrome. The present study is the first clinical trial that evaluated the effects of zinc supplementation on metabolic and oxidative stress status in overweight/obese patients with NAFLD undergoing calorie- restriction diet. Methods: Fifty six overweight/obese patients with confirmed mild to moderate NAFLD using ultrasonography were randomly allocated to receive 30 mg elemental zinc supplement (n = 29) or placebo (n = 27) along with weight loss diet for 12 weeks. Serum levels of zinc, homeostasis model of assessment-estimated insulin resistance (HOMA-IR), lipid profile, serum superoxide dismutas1 (SOD1) and malondialdhyde (MDA) levels were assessed. ResultsSerum levels of insulin, SOD1, MDA and HOMA-IR were improved in the treatment group (p < 0.05). Within group comparison showed significant reduction in serum FBS, HbA1C, TC, LDL-c and TG in the treatment group. Conclusion: Zinc supplementation for three months improved insulin resistance and oxidative stress status in overweight/obese NAFLD patients with no beneficial effects on lipid profiles over weight loss diet. Registration ID in IRCT (IRCT NO: 20181005041238N1).

Biomarkers of Oxidative Stress in Metabolic Syndrome and Associated Diseases.

Metabolic syndrome (MS) represents worldwide public health issue characterized by a set of cardiovascular risk factors including obesity, diabetes, dyslipidemia, hypertension, and impaired glucose tolerance. The link between the MS and the associated diseases is represented by oxidative stress (OS) and by the intracellular redox imbalance, both caused by the persistence of chronic inflammatory conditions that characterize MS. The increase in oxidizing species formation in MS has been accepted as a major underlying mechanism for mitochondrial dysfunction, accumulation of protein and lipid oxidation products, and impairment of the antioxidant systems. These oxidative modifications are recognized as relevant OS biomarkers potentially able to (i) clarify the role of reactive oxygen and nitrogen species in the etiology of the MS, (ii) contribute to the diagnosis/evaluation of the disease's severity, and (iii) evaluate the utility of possible therapeutic strategies based on natural antioxidants. The antioxidant therapies indeed could be able to (i) counteract systemic as well as mitochondrial-derived OS, (ii) enhance the endogenous antioxidant defenses, (iii) alleviate MS symptoms, and (iv) prevent the complications linked to MS-derived cardiovascular diseases. The focus of this review is to summarize the current knowledge about the role of OS in the development of metabolic alterations characterizing MS, with particular regard to the occurrence of OS-correlated biomarkers, as well as to the use of therapeutic strategies based on natural antioxidants.

Betulinic acid improves insulin sensitivity, hyperglycemia, inflammation and oxidative stress in metabolic syndrome rats via PI3K/Akt pathways

This study investigated the influence of betulinic acid on high-fructose diet-induced metabolic syndrome in rats. Oral administration of betulinic acid significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, betulinic acid restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Betulinic acid-mediated upregulation of protein kinase B (Akt) and phosphoinositde-3 kinase (PI3K) anulled high-fructose diet mediated depletion. Also, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of betulinic acid restored high-fructose diet-mediated increase in the levels of lipid profile parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. Conclusively, betulinic acid improves insulin sensitivity, elevated blood glucose, inflammation and dyslipidaemia and oxidative stress in high-fructose diet-induced metabolic syndrome through the PI#Kand Akt pathways .

PO-250 Exercise and dietary intervention reduce myocardial oxidative stress in male rats with metabolic syndrome

Objective Both aerobic exercise and alimentary control relieve oxidative stress (OS). However, there may be different modes. The objective of this study is to identify the effects of OS in metabolic syndrome (MS) rats and explore the mechanisms involved in aerobic exercise and alimentary control.&#x0D; Methods Seventy rats were used. Eight rats were randomly chosen for the control group, while the remaining rats were subjected to MS using a high-fat diet for 18 wk. The MS model rats were subsequently divided into the MHC (model control with high-fat diet), MRC (model control with routine diet), MHE (model training with high-fat diet) and MRE (model training routine diet) groups for 12 wk. The chemotactic factor macrophage chemoattractant protein-1 (MCP-1), the adherence factor plasminogen activator inhibitor I (PAI-1), the oxidative stressor oxidized low density lipoprotein (ox-LDL), and the antioxidative factor endothelial nitric oxide synthase (eNOS) were tested in the serum; moreover, the expressions of MCP-1, PAI-1, and eNOS and the regulatory factor of OS Peroxisome proliferator-activated receptor-alpha (PPARα) were detected in the myocardium.&#x0D; Results OS related markers in serum had changes following the interventions of aerobic exercise and/or diet control. Compared with C, the ox-LDL, MCP-1 and PAI-1 in the MS rats exhibited significant decreases (P＜0.05/0.01), and the eNOS had a significant increase (P＜0.05). Compared with MHC, the diet intervention alone significantly increased eNOS; when interventions of aerobic exercise but not diet control (MHE) were applied, they significantly decreased ox-LDL, MCP-1 and PAI-1 (P＜0.01); the applied interventions of both aerobic exercise and diet control (MRE) decreased ox-LDL, MCP-1 and PAI-1 and significantly decreased eNOS (P＜0.01). The MRE compared to MHE exhibited significant changes in MCP-1 and eNOS (P＜0.01). The mRNA levels of the processing markers of OS in the myocardium. Compared with C, the MS rats had significant increases in the chemotactic factor MPC-1 (P＜0.05) and the adhesion factor PAI-1 (P＜0.01), which indicated that MS rats exhibited enhanced OS. Moreover, the MS rats had an increased antioxidant marker of eNOS, which was not significant, and the regulatory factor of PPARα decreased (P＜0.01). Compared to MHC, the MRC rats exhibited decreased MPC-1 (P＞0.05) and PAI-1 (P＜0.05) and increased eNOS (P＜0.01) and PPARα (P＞0.05); moreover, the MHE and MRE rats decreased more in MPC-1 and PAI-1 (P＜0.01) with increased eNOS and PPARα (P＜0.01). Compared to MHE, the MRE rats had a further decrease in MPC-1 (P＜0.01) and PAI-1 (P＞0.05) with increased eNOS (P＜0.05) and PPARα (P＞0.05).&#x0D; Conclusions OS increased in MS rats. Moreover, aerobic exercise and alimentary control could decrease OS to reduce the damage in MS rats. The OS regulatory factor PPARα, which could mediate the expression of OS-related genes, such as MCP-1, PAI-1, and eNOS in cardiovascular tissues, was only enhanced by aerobic exercise and not by diet control.

Oxidative stress in metabolic syndrome & its association with DNA-strand break.

Background & objectives:Oxidative stress (OS) is associated with numerous components of metabolic syndrome (MetS). This study was aimed to investigate if hydrogen peroxide (H2O2) as the reactive oxygen species was capable of depicting OS in MetS, and If MetS patients showed DNA damage in the form of DNA strand breaks (DSB).Methods:A total of 160 participants (90 males, 70 females) ≥20 yr of age were categorized into four groups based on the number of MetS risk parameters (n=40 in each group). Sugar and lipid profile, H2O2 concentration in blood and DNA-strand breaks were measured.Results:DSB was significantly more in those with MetS (n=40) than those without (n=120) whereas H2O2 levels were the same in both the study groups. The number of DSB differed significantly between the control and 3 risk factor groups. DSB was also higher in groups with 2 and 1 risk factors compared to 0 risk but the difference was not significant. H2O2 level was higher in groups with 3, 2 and 1 risk factors compared to 0 risk group but the difference was not significant. The H2O2 level correlated positively with triglyceride values but not with other MetS risk parameters. There was no significant correlation between DSB and MetS risk parameters.Interpretation & conclusions:Our findings showed a cumulative and synergistic effect of the risk factors of MetS on DSB. Individuals with three risk parameters had a greater effect on DNA damage than in those with two or one risk parameter. Although plasma H2O2 level increased with an increase in the fat depots, use of H2O2 to depict OS in MetS should be coupled with an adjunct and estimation of DSB in peripheral blood lymphocytes may be used as indicator of OS in MetS patients.

Myelo peroxidase as an Indicator of Oxidative Stress in Metabolic Syndrome

Background: Increased myeloperoxidase (MPO) activity would be the link between the rise of the inflammatory response and oxidative stress (OS) in metabolic syndrome (MS). Objective: The aim of this study was to determine the enzymatic activity of MPO associated with OS in animals with MS and establish their relationship with probable cardiovascular injury. Methods: Male Wistar rats were divided into two groups: Group A, control (n=12) and Group B, induced MS (n=12). Metabolic syndrome was produced by 6-week administration of 10% fructose diluted in the drinking water. Insulin (mU/ml), glucose (mg/dl), lipid panel (mg/dl), HOMA (homeostatic model assessment), MPO (IU/ml) and superoxide dismutase (SOD) activity (U/ml) were measured. Light microscopy was used for the histological study of the heart and thoracic aorta. Results: Group B showed significantly increased levels of plasma glucose (176±17.3 mg/dl), insulin (29.5±4.52 mU/ml), HOMA (11±1.3), total cholesterol (133±9.6 mg/dl) and triglycerides (75±12.9 mg/dl) compared with Group A: plasma glucose (115±1.1 mg/dl), insulin (4±0.82 mU/ml), HOMA (3±0.38), total cholesterol (69.7±1.6 mg/dl) and triglycerides (46.2±6 mg/dl), (p<0.001 for all variables). A significant decrease in HDL (28.3±1.14 mg/dl) in Group B vs. Group A (61±1.0 mg/dl) (p<0.001) validated the experimental MS model. Myeloperoxidase activity increased significantly in Group B (181.3±15.7 IU/ml) vs. Group A (116.07±4.2 IU/ml) (p<0.001). A similar behavior was seen with SOD antioxidant activity in Group B (181±6 U/ml) vs. Group A (138±3.6 U/ml) (p <0.01). Light microscopy of the heart and thoracic aorta revealed histopathological changes in animals with induced MS. Conclusion: Increased MPO and SOD in Group B would indicate the presence of OS in MS, with consequences at the vascular level.

Evaluation of Cardio Metabolic Profile, Endothelial Dysfunction and Oxidative Stress in Metabolic Syndrome:A Comparative Perspective

Evaluation of Cardio Metabolic Profile, Endothelial Dysfunction and Oxidative Stress in Metabolic Syndrome:A Comparative Perspective

Oxidative Inactivation of Liver Mitochondria in High Fructose Diet-Induced Metabolic Syndrome in Rats: Effect of Glycyrrhizin Treatment.

Metabolic syndrome is a serious health problem in the present world. Glycyrrhizin, a triterpenoid saponin of licorice (Glycyrrhiza glabra) root, has been reported to ameliorate the primary complications and hepatocellular damage in rats with the syndrome. In this study, we have explored metabolic syndrome-induced changes in liver mitochondrial function and effect of glycyrrhizin against the changes. Metabolic syndrome was induced in rats by high fructose (60%) diet for 6 weeks. The rats were then treated with glycyrrhizin (50 mg/kg body weight) by single intra-peritoneal injection. After 2 weeks of the treatment, the rats were sacrificed to collect liver tissue. Elevated mitochondrial ROS, lipid peroxidation and protein carbonyl, and decreased reduced glutathione content indicated oxidative stress in metabolic syndrome. Loss of mitochondrial inner membrane cardiolipin was observed. Mitochondrial complex I activity did not change but complex IV activity decreased significantly. Mitochondrial MTT reduction ability, membrane potential, phosphate utilisation and oxygen consumption decreased in metabolic syndrome. Reduced mitochondrial aconitase activity and increased aconitase carbonyl content suggested oxidative damage of the enzyme. Elevated Fe(2+) ion level in mitochondria might be associated with increased ROS generation in metabolic syndrome. Glycyrrhizin effectively attenuated mitochondrial oxidative stress and aconitase degradation, and improved electron transport chain activity. Copyright © 2016 John Wiley & Sons, Ltd.

Metabolic Syndrome: An Important Risk Factor for Parkinson’s Disease

Metabolic syndrome is becoming commoner due to a rise in obesity rates among adults. Generally speaking, a person with metabolic syndrome is twice as likely to develop cardiovascular disease and five times as likely to develop diabetes as someone without metabolic syndrome. Increasing oxidative stress in metabolic syndrome and Parkinson's disease is mentioned in the comprehensive articles; however, the system review about clear relation between metabolic syndrome and Parkinson's disease is deficient. In this review, we will focus on the analysis that the metabolic syndrome may be a risk factor for Parkinson's disease and the preventions that reduce the incident of Parkinson's disease by regulating the oxidative stress.

Emerging role of oxidative stress in metabolic syndrome and cardiovascular diseases: important role of Rac/NADPH oxidase

'Oxidative stress' is a term defining states of elevated reactive oxygen species (ROS) levels. Normally, ROS control several physiological processes, such as host defence, biosynthesis of hormones, fertilization and cellular signalling. However, oxidative stress has been involved in different pathologies, including metabolic syndrome and numerous cardiovascular diseases. A major source of ROS involved in both metabolic syndrome and cardiovascular pathophysiology is the NADPH oxidase (NOX) family of enzymes. NOX is a multi-component enzyme complex that consists of membrane-bound cytochrome b-558, which is a heterodimer of gp91phox and p22phox, cytosolic regulatory subunits p47phox and p67phox, and the small GTP-binding protein Rac1. Rac1 plays many important biological functions in cells, but perhaps the most unique function of Rac1 is its ability to bind and activate the NOX complex. Furthermore, Rac1 has been reported to be a key regulator of oxidative stress through its co-regulatory effects on both nitric oxide (NO) synthase and NOX. Therefore, the main goal of this review is to give a brief outline about the important role of the Rac1-NOX axis in the pathophysiology of both metabolic syndrome and cardiovascular disease.