Oxidative stress and high-density lipoprotein function in Type I diabetes and end-stage renal disease

2005 ◽  
Vol 108 (6) ◽  
pp. 497-506 ◽  
Author(s):  
George KALOGERAKIS ◽  
Arthur M. BAKER ◽  
Steve CHRISTOV ◽  
Kevin G. ROWLEY ◽  
Karen DWYER ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Protein ◽  
Healthy Subjects ◽  
Type I Diabetes ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Pon1 Activity ◽  
Type I

In a cross-sectional study, oxidative stress in high vascular disease risk groups, ESRD (end-stage renal disease) and Type I diabetes, was assessed by measuring plasma protein carbonyls and comparing antioxidant capacity of HDL (high-density lipoprotein) as pertaining to PON1 (paraoxonase 1) activity and in vitro removal of LPO (lipid peroxides). ESRD subjects on haemodialysis (n=22), Type I diabetes subjects (n=20) without vascular complications and healthy subjects (n=23) were compared. Plasma protein carbonyls were higher in ESRD patients [0.16 (0.050) nmol/mg of protein; P=0.001; value is mean (SD)] relative to subjects with Type I diabetes [0.099 (0.014) nmol/mg of protein] and healthy subjects [0.093 (0.014) nmol/mg of protein]. Plasma PON1 activity, with and without correction for HDL-cholesterol, was lower in diabetes but did not differ in ESRD compared with healthy subjects. Plasma PON1 activity, without correction for HDL, did not differ between the three groups. In ESRD, plasma PON1 activity and plasma protein carbonyl concentrations were inversely related (r=−0.50, P<0.05). In an in vitro assay, LPO removal by HDL in ESRD subjects was greater than HDL from healthy subjects (P<0.01), whereas HDL from patients with Type I diabetes was less effective (P<0.01). Efficacy of LPO removal was unrelated to plasma PON1 activity, in vitro glycation or mild oxidation, but was impaired by marked oxidation and glycoxidation. Protein carbonyl levels are increased in ESRD but not in complication-free Type I diabetes. HDL antioxidant function is increased in ESRD, perhaps a compensatory response to increased oxidative stress, but is lower in Type I diabetes. HDL dysfunction is related to glycoxidation rather than glycation or PON1 activity.

scholarly journals Protective effect of essential oil of Cinnamomum verum bark on hepatic and renal toxicity induced by carbon tetrachloride in rats

2019 ◽  
Vol 44 (6) ◽  
pp. 606-618 ◽  
Author(s):  
Khaled Bellassoued ◽  
Ferdaws Ghrab ◽  
Houda Hamed ◽  
Rim Kallel ◽  
Jos van Pelt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Renal Toxicity ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Untreated Group ◽  
Protective Effects ◽  
Glutamyl Transferase

The inner bark of cinnamon (Cinnamomum verum) is widely used as a spice. Cinnamon plants are also a valuable source of essential oil used for medicinal purposes. The present study aimed to investigate the composition and in vitro antioxidant activity of essential oil of C. verum bark (CvEO) and its protective effects in vivo on CCl4-induced hepatic and renal toxicity in rats. Groups of animals were pretreated for 7 days with CvEO (70 or 100 mg/kg body weight) or received no treatment and on day 7 a single dose of CCl4 was used to induce oxidative stress. Twenty-four hours after CCl4 administration, the animals were euthanized. In the untreated group, CCl4 induced an increase in serum biochemical parameters and triggered oxidative stress in both liver and kidneys. CvEO (100 mg/kg) caused significant reductions in CCl4-elevated levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyl transferase, lactate dehydrogenase, total cholesterol, triglycerides, low-density lipoprotein, urea, and creatinine and increased the level of high-density lipoprotein compared with the untreated group. Moreover, pretreatment with CvEO at doses of 70 and 100 mg/kg before administration of CCl4 produced significant reductions in thiobarbituric acid reactive substances and protein carbonyl levels in liver and kidney tissues compared with the untreated group. The formation of pathological hepatic and kidney lesions induced by the administration of CCl4 was strongly prevented by CvEO at a dose of 100 mg/kg. Overall, this study suggests that administration of CvEO has high potential to quench free radicals and alleviate CCl4-induced hepatorenal toxicity in rats.

High-density lipoprotein composition and paraoxonase activity in Type I diabetes

2001 ◽  
Vol 101 (6) ◽  
pp. 659-670 ◽  
Author(s):  
Jonathan VALABHJI ◽  
Avril J. McCOLL ◽  
Michael SCHACHTER ◽  
Surinder DHANJIL ◽  
William RICHMOND ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Particle Density ◽  
Type I Diabetes ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
Cholesterol Concentration ◽  
Pon1 Activity ◽  
Type I ◽  
Carotid Imt

Type I diabetes is associated with a high incidence of coronary heart disease (CHD), despite a normal or even increased concentration of high-density lipoprotein (HDL) cholesterol. This paradox may be explained by changes in the antioxidant capacity of HDL, related to paraoxonase (PON1) activity. HDL compositional changes in subjects with Type I diabetes may result in changes in PON1 activity that are associated with a higher incidence of CHD. Single-vertical-spin density-gradient ultracentrifugation was used to isolate seven HDL fractions from serum according to density. PON1 activity was measured in serum and in the HDL fractions using phenyl acetate as substrate. The mean recovery of PON1 activity in the HDL fractions was 87% (S.D. 12%). CHD risk was assessed using B-mode ultrasound to measure carotid artery intima-media thickness (IMT). Groups of 35 subjects with Type I diabetes {duration of diabetes 18 years (12-32 years) [median (interquartile range)]; glycated haemoglobin 7.67% (1.17%)} and 24 non-diabetic control subjects were studied. Carotid IMT was greater in the diabetic subjects [0.60 (0.55-0.70) compared with 0.55 (0.45-0.64) mm; P = 0.042] and HDL cholesterol concentration was higher [1.53 (0.36) compared with 1.32(0.34)mmol/l; P = 0.031]. There were qualitative differences in HDL in subjects with Type I diabetes: HDL particles were triacylglycerol-deplete, and there were greater numbers of the larger, more buoyant HDL particles. These properties were not those found to determine PON1 activity. PON1 activity increased as HDL particle density increased and particle size decreased; the increase in PON1 activity was associated with an increase in the ratio of the two HDL surface lipid components, phospholipid and unesterified cholesterol, as particle density increased. PON1 activity was similar in diabetic and non-diabetic subjects [121 (28) and 120 (36)μmolċmin-1ċml-1 respectively; P = 0.887]. PON1 activity was not associated with carotid IMT in either group. Our results suggest that the PON1 activities of HDL particles relate to the density, size and composition of the particles. However, PON1 activity does not appear to contribute to the greater risk of CHD in subjects with Type I diabetes.

Protective effect of resveratrol on formation of membrane protein carbonyls and lipid peroxidation in erythrocytes subjected to oxidative stress

2009 ◽  
Vol 34 (6) ◽  
pp. 1093-1097 ◽  
Author(s):  
Kanti Bhooshan Pandey ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Carbonyl Group ◽  
Antioxidant Properties ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Beneficial Effects ◽  
Group Content ◽  
Tert Butylhydroperoxide ◽  
Protein Carbonyl Group

Many of the biological actions of resveratrol have been attributed to its antioxidant properties. In this work, we subjected human erythrocytes to in vitro oxidative stress by incubating them with tert-butylhydroperoxide (t-BHP). This caused a significant increase in the malondialdehyde (MDA) level and the protein carbonyl group content above the basal values. The presence of trans-resveratrol at micromolar concentrations in the incubation medium protected the erythrocytes from t-BHP-induced oxidative stress, as evidenced by the decrease in the MDA level and the protein carbonyl group content. The effect of resveratrol was concentration and time-dependent. Our findings help to explain some of the beneficial effects of resveratrol.

Effects of olive oil and its minor constituents on serum lipids, oxidative stress, and energy metabolism in cardiac muscle

2006 ◽  
Vol 84 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Luciane A. Faine ◽  
Hosana G. Rodrigues ◽  
Cristiano M. Galhardi ◽  
Geovana M.X. Ebaid ◽  
Yeda S. Diniz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Energy Metabolism ◽  
Olive Oil ◽  
Cardiac Muscle ◽  
Serum Lipids ◽  
Virgin Olive Oil ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Lipid Hydroperoxides

Recent lines of evidence suggest that the beneficial effects of olive oil are not only related to its high content of oleic acid, but also to the antioxidant potential of its polyphenols. The aim of this work was determine the effects of olive oil and its components, oleic acid and the polyphenol dihydroxyphenylethanol (DPE), on serum lipids, oxidative stress, and energy metabolism on cardiac tissue. Twenty four male Wistar rats, 200 g, were divided into the following 4 groups (n = 6): control (C), OO group that received extra-virgin olive oil (7.5 mL/kg), OA group was treated with oleic acid (3.45 mL/kg), and the DPE group that received the polyphenol DPE (7.5 mg/kg). These components were administered by gavage over 30 days, twice a week. All animals were provided with food and water ad libitum The results show that olive oil was more effective than its isolated components in improving lipid profile, elevating high-density lipoprotein, and diminishing low-density lipoprotein cholesterol concentrations. Olive oil induced decreased antioxidant Mn-superoxide dismutase activity and diminished protein carbonyl concentration, indicating that olive oil may exert direct antioxidant effect on myocardium. DPE, considered as potential antioxidant, induced elevated aerobic metabolism, triacylglycerols, and lipid hydroperoxides concentrations in cardiac muscle, indicating that long-term intake of this polyphenol may induce its undesirable pro-oxidant activity on myocardium.

scholarly journals Glycyrrhizic acid ameliorates submandibular gland oxidative stress, autophagy and vascular dysfunction in rat model of type 1 diabetes

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Saad Mohamed Asseri ◽  
Nehal M. Elsherbiny ◽  
Mohamed El-Sherbiny ◽  
Iman O. Sherif ◽  
Alsamman M. Alsamman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Glycyrrhizic Acid ◽  
Type I Diabetes ◽  
Vascular Dysfunction ◽  
Type I ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Ameliorative Effect ◽  
Related Proteins

AbstractThe burden of diabetes mellitus (DM) and associated complications is increasing worldwide, affecting many organ functionalities including submandibular glands (SMG). The present study aims to investigate the potential ameliorative effect of glycyrrhizic acid (GA) on diabetes-induced SMG damage. Experimental evaluation of GA treatment was conducted on a rat model of type I diabetes. Animals were assigned to three groups; control, diabetic and GA treated diabetic groups. After 8 weeks, the SMG was processed for assessment of oxidative stress markers, autophagy related proteins; LC3, Beclin-1 and P62, vascular regulator ET-1, aquaporins (AQPs 1.4 and 5), SIRT1 protein expressions in addition to LC3 and AQP5 mRNA expressions. Also, parenchymal structures of the SMG were examined. GA alleviated the diabetes-induced SMG damage via restoring the SMG levels of oxidative stress markers and ET-1 almost near to the normal levels most probably via regulation of SIRT1, AQPs and accordingly LC-3, P62 and Beclin-1levels. GA could be a promising candidate for the treatment of diabetes-induced SMG damage via regulating oxidative stress, autophagy and angiogenesis.

scholarly journals Protein carbonyls and protein thiols in rheumatoid arthritis

2018 ◽  
Vol 6 (5) ◽  
pp. 1738 ◽  
Author(s):  
Pullaiah P. ◽  
Suchitra M. M. ◽  
Siddhartha Kumar B.
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Protein Modification ◽  
Antioxidant Properties ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Carbonyl Content ◽  
Protein Thiol ◽  
Protein Carbonyl Content ◽  
Protein Thiols

Background: Oxidative stress (OS) has an important role in the pathogenesis and progression of rheumatoid arthritis (RA). OS causes protein modification, thereby impairing the biological functions of the protein. This study was conducted to assess the oxidatively modified protein as protein carbonyl content and the antioxidant status as protein thiols, and to study the association between protein carbonyls and protein thiols in RA.Methods: Newly diagnosed RA patients who were not taking any disease modifying anti-rheumatic drugs were included into the study group (n=45) along with age and sex matched healthy controls (n=45). Serum protein carbonyl content and protein thiols were estimated.Results: Elevated protein carbonyl content and decreased protein thiol levels (p<0.001) were observed in RA. A significant negative correlation was observed between protein carbonyl content and protein thiol levels (p<0.001).Conclusions: Oxidative stress in RA is evidenced by enhanced protein oxidation and decreased antioxidant protein thiol levels. Decreased protein thiols may also reflect protein modifications leading to compromise in the antioxidant properties. This oxidant and antioxidant imbalance needs to be addressed by therapeutic interventions to prevent disease progression.

scholarly journals Raphanus sativus ameliorates atherogeneic lipid profiles in hypercholesterolemic rats and hypercholesterolemia-associated peroxidative liver damage

2011 ◽  
Vol 7 (3) ◽  
pp. 1385-1394 ◽  
Author(s):  
Mozammel Haque ◽  
Jahirul Islam ◽  
Asiqur Rahaman ◽  
Fowzia Akter Selina ◽  
Mohammad Azizur Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Raphanus Sativus ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Water Extract ◽  
Density Lipoprotein ◽  
Lipid Peroxide ◽  
Hot Water

Objective: Raphanus sativus is a hugely used edible root vegetable. We investigated whether the feeding of the Raphanus sativus hot water extract (RSE) ameliorates atherogenic lipid profile and oxidative stress in hypercholesterolemia. Methods: After feeding of the RSE to hypercholesterolemic rats for 6 weeks, the levels of plasma and hepatic total cholesterol (TC), triglyceride (TG), and plasma high density lipoprotein-cholesterol (HDL-C) and fecal TC levels were studied. The effects of RSE on the hepatic enzymes, namely alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), the levels of lipid peroxide (LPO) and liver histology were also evaluated. Results: Hypercholesterolemia increased the levels of TC and TG in the plasma and livers. The levels of ALT, AST and ALP in plasma and LPO in the liver also increased. The dietary RSE, however, significantly ameliorated the above atherogenic lipids and liver enzymes. The RSE significantly reduced the levels of LPO in the liver, suggesting an in vivo protection against of oxidative stress. The RSE also inhibited the in vitro Fenton’s reagent-induced oxidative stress, thus corroborating the in vivo anti-LPO actions of RSE. The levels of hepatic LPO were positively correlated with plasma AST (r=0.76; P <0.05) and ALT (r=0.43; P<0.05) levels. Histologically, the livers of the RSE-fed hypercholesterolemic rats exhibited lesser fatty droplets and reduced inflammatory cells. Conclusion: Finally, R. sativus extract lowers the cardiovascular disease risk factors under hypercholesterolemic situation by increasing the plasma/hepatic clearance of cholesterol and improving the hypercholesterolemia-induced oxidative damage of hepatic tissues.

scholarly journals Serum Fetuin-B Levels Are Elevated in Women with Metabolic Syndrome and Associated with Increased Oxidative Stress

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Shiyao Xue ◽  
Hongdong Han ◽  
Shunli Rui ◽  
Mengliu Yang ◽  
Yizhou Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Healthy Subjects ◽  
Bioinformatics Analysis ◽  
Cholesterol Metabolism ◽  
In Vitro Study ◽  
Multivariate Regression Analysis ◽  
Regulatory Factors ◽  
Triglyceride Content

Previous studies on serum fetuin-B (fetuin-like protein IRL685) have investigated its association with T2DM; however, the reason for the variation in serum fetuin-B and its regulatory factors in metabolic disease remain unclear. Here, we evaluated serum fetuin-B levels in women with newly diagnosed MetS and performed multiple interventions to investigate the role of fetuin-B in the pathogenesis of MetS. Serum fetuin-B levels were assessed using ELISA. Bioinformatics analysis was performed to analyze fetuin-B-related genes and signaling pathways. Additionally, oxidative stress parameters were measured in the in vitro study. For subgroup analyses, we performed EHC, OGTT, and treatment with a GLP-1RA to investigate the regulatory factors of serum fetuin-B. We found that in comparison with healthy subjects, serum fetuin-B levels were markedly increased in women with MetS. Further, serum fetuin-B showed a positive correlation with WHR, FAT%, TG, FBG, HbA1c, FIns, HOMA-IR, VAI, and LAP. Bioinformatics analysis revealed that most fetuin-B-related core genes were involved in cholesterol metabolism and fat decomposition. Consistent with this finding, multivariate regression analysis showed that triglyceride content and WHR were independently associated with serum fetuin-B. We also observed that serum fetuin-B levels were markedly elevated in healthy subjects after glucose loading and in women with MetS during EHC. In vitro, overexpression of fetuin-B promoted oxidative stress in HepG2 cell. After 6 months of treatment with a GLP-1RA, serum fetuin-B levels in women with MetS decreased following an improvement in metabolism and insulin sensitivity. Therefore, serum fetuin-B is associated with MetS, which may serve as a biomarker of oxidative stress. This trial is registered with ChiCTR-OCC-11001422.

Abstract 628: Hepatic Insulin Signaling Regulates ApoA-I Gene Expression Through the Type I Deiodinase.

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Jing Liu ◽  
Antonio Hernandez-Ono ◽  
Valerie Galton ◽  
Henry Ginsberg
Keyword(s):  
Insulin Signaling ◽  
Knockout Mice ◽  
Hepg2 Cells ◽  
Density Lipoprotein ◽  
Type I ◽  
Mrna Levels ◽  
Reverse T3 ◽  
Hepatic Insulin Signaling ◽  
Low Levels

People with low levels of high density lipoprotein cholesterol (HDLC) and apolipoprotein A-I (ApoA-I) have a higher risk of cardiovascular disease. Low levels of HDLC are common in individuals who are insulin resistant (IR), e.g., with metabolic syndrome and type 2 diabetes mellitus (T2DM). Despite the high prevalence of these two disorders, very little work has been reported regarding the molecular pathways linking insulin signaling or action and the levels of either HDLC or ApoA-1. We reported previously that liver specific insulin receptor (InsR) knockout mice (LIRKO) have markedly reduced plasma HDLC levels that increase after restoration of hepatic Akt signaling. In the present study, we created acute LIRKO mice by injecting an albumin-Cre adenovirus (Ad) into InsR floxed mice and observed marked reductions in HDLC, the expression of ApoA-I, and the expression of the gene coding Type1 iodothyronine deiodinase1, a selenoenzyme expressed highly in the liver that converts thyroxine to 3,5,3’-triiodothyronine (T3) or reverse T3. Deiodinase 1 knockout mice also had significantly reduced hepatic ApoA-I mRNA levels. Overexpression of Dio1 in LIRKO restored HDLC and significantly increased the expression of ApoA-I mRNA. In vitro studies showed that the expression of ApoA-I was significantly reduced after knockdown of either InsR or Dio1 expression in HepG2 cells. Moreover, overexpression of Dio1 restored ApoA-I promoter activity that had been decreased by knockdown of InsR. Deletion analysis of ApoAI promoter regions showed that insulin signaling regulated ApoA-I expression by acting on a region which does not contain any thyroid response elements. Pulse-chase experiments in HepG2 cells showed that deficiency of insulin signaling resulted in decreased synthesis and secretion of ApoAI. Our results indicates that defective hepatic insulin signaling results in reduced expression of Dio1 which, in turn, leads to reduced expression of ApoA-I and decreased synthesis and secretion of ApoA-I from hepatocytes. We believe our studies have defined a novel pathway from insulin signaling to ApoA-I synthesis that may lead to new approaches for increasing HDL levels in people with defective insulin signaling.

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