scholarly journals Cuminum cyminum methanolic extract prevents oxidative modification of low density lipoproteins: Preliminary evidence on its anti-atherosclerotic potential

2018 ◽  
Vol 7 (1) ◽  
pp. 79-83
Author(s):  
Ranjitsinh Devkar ◽  
◽  
Kiran Lagu ◽  
Jaymesh Thadani ◽  
Kavita Shirsath ◽  
...  
Keyword(s):  
Methanolic Extract ◽  
Ex Vivo ◽  
Lipid Hydroperoxide ◽  
Oxidation Kinetic ◽  
Preliminary Evidence ◽  
Oxidative Modification ◽  
Oxidation Products ◽  
Ldl Oxidation ◽  
Efficient Treatment ◽  
Cuminum Cyminum

The significance of oxidative modification of LDL in the pathogenesis of atherosclerosis and the lack of efficient treatment intervention has led researchers to develop an effective therapy based on natural antioxidants. The present study provides preliminary evidence in support of the anti-atherosclerotic potential of methanolic extract of Cuminum cyminum L. (CC). We found that CC inhibited Cu2+ -mediated LDL oxidation as demonstrated by the ex vivo LDL oxidation kinetic study, the LDL oxidation products (malondialdehyde, lipid hydroperoxide and protein carbonyl), and ApoB fragmentation assay. It can be concluded that, CC efficiently alleviates experimentally induced oxidative changes and modifications of LDL. Since oxidative changes in LDL are prerequisite to onset of atherogenic changes, this study provides preliminary evidence on anti-atherosclerotic potential of CC

scholarly journals Lipoxygenase treatment render low-density lipoprotein susceptible to Cu2+-catalysed oxidation

1996 ◽  
Vol 314 (2) ◽  
pp. 577-585 ◽  
Author(s):  
Achim LASS ◽  
Jutta BELKNER ◽  
Hermann ESTERBAUER ◽  
Hartmut KÜHN
Keyword(s):  
Low Density Lipoprotein ◽  
Complex Mixture ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Oxidation Products ◽  
Ldl Oxidation ◽  
Foam Cell Formation ◽  
Low Density ◽  
Catalysed Oxidation ◽  
Lag Period

Oxidative modification of low-density lipoprotein (LDL) has been implicated in foam-cell formation at all stages of atherosclerosis. Since transition metals and mammalian 15-lipoxygenases are capable of oxidizing LDL to its atherogenic form, a concerted action of these two catalysts in atherogenesis has been suggested. Cu2+-catalysed LDL oxidation is characterized by a kinetic lag period in which the lipophilic antioxidants are decomposed and by a complex mixture of unspecific oxidation products. We investigated the kinetics of the 15-lipoxygenase-catalysed oxygenation of LDL and found that the enzyme is capable of oxidizing LDL in the presence of the endogenous lipophilic antioxidants. In contrast with the Cu2+-catalysed reaction, no kinetic lag phase was detected. The pattern of products formed during short-term incubations was highly specific, with cholesterol-esterified (13S)-hydroperoxy-(9Z,11E)-octadecadienoic acid being the major product. However, after long-term incubations the product pattern was less specific. Preincubation with 15-lipoxygenase rendered human LDL more susceptible to Cu2+-catalysed oxidation as indicated by a dramatic shortening of the lag period. Addition of Cu2+ to lipoxygenase-treated LDL led to a steep decline in its antioxidant content and to a greatly reduced lag period. Interestingly, if normalized to a comparable hydroperoxide content, autoxidation and addition of exogenous hydroperoxy fatty acids both failed to overcome the lag period. The local peroxide concentrations in various LDL subcompartments will be discussed as a possible reason for this unexpected behaviour.

scholarly journals Salivary Antioxidants and Oxidative Stress in Psoriatic Patients: Can Salivary Total Oxidant Status and Oxidative Status Index Be a Plaque Psoriasis Biomarker?

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Anna Skutnik-Radziszewska ◽  
Mateusz Maciejczyk ◽  
Katarzyna Fejfer ◽  
Julita Krahel ◽  
Iwona Flisiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plaque Psoriasis ◽  
Healthy Subjects ◽  
Lipid Hydroperoxide ◽  
Oxidative Status ◽  
Oxidative Modification ◽  
Oxidation Products ◽  
Stress Index ◽  
Study Group ◽  
Lipid Oxidation Products

The aim of our research was to evaluate redox balance parameters and biomarkers of oxidative stress (OS) in nonstimulated and stimulated saliva as well as the blood of patients with plaque psoriasis compared to healthy controls. The study involved 40 patients with plaque psoriasis and 40 generally healthy subjects matched by age and gender to the study group patients. We assayed the concentration/activity of antioxidant enzymes: salivary peroxidase (Px), catalase (CAT), and superoxide dismutase (SOD) measured in unstimulated saliva (NWS), stimulated saliva (SWS), and erythrocytes. In plasma as well as NWS and SWS, we measured the concentration/activity of reduced glutathione (GSH), total antioxidant potential (TAC), total oxidative status (TOS), oxidative stress index (OSI), and markers of oxidative modification of proteins: advanced glycation end products (AGE), advanced oxidation protein products (AOPP), and lipid oxidation products: malondialdehyde (MDA) and total lipid hydroperoxide (LOOH). In NWS and SWS, we also evaluated the rate of reactive oxygen species (ROS) production. The concentration of Px, CAT, and SOD was significantly higher in NWS of patients with plaque psoriasis vs. healthy subjects. In SWS of psoriatic patients, we observed considerably higher concentration of Px and CAT, and in erythrocytes of patients with plaque psoriasis, the concentration of GPx and CAT was significantly higher compared to that in the controls. The levels of AOPP, AGE, MDA, and LOOH were considerably higher in NWS, SWS, and plasma of the study group compared to the controls. The concentration of total protein and salivary amylase was significantly lower in NWS and SWS of psoriatic patients compared to the healthy control. In the course of plaque psoriasis, we observed redox imbalances with prevalence of oxidation reactions. Mechanisms involved in the synthesis/secretion of proteins and activity of amylase were depressed in both glands of psoriatic patients; however, they were more inhibited in the parotid gland compared to the submandibular gland. TOS concentration and OSI value in NWS and SWS may serve as diagnostic biomarkers of plaque psoriasis.

scholarly journals Attenuation of diabetic complications by C-phycoerythrin in rats: antioxidant activity of C-phycoerythrin including copper-induced lipoprotein and serum oxidation

2009 ◽  
Vol 102 (1) ◽  
pp. 102-109 ◽  
Author(s):  
Badrish Soni ◽  
Nishant P. Visavadiya ◽  
Datta Madamwar
Keyword(s):  
Body Weight ◽  
Diabetic Complications ◽  
Ex Vivo ◽  
Lipid Hydroperoxide ◽  
Male Rats ◽  
Ldl Oxidation ◽  
Lag Phase ◽  
Significant Prolongation ◽  
Reducing Ability

In the present study, the protective role of purified C-phycoerythrin (C-PE) against diabetic complications and Cu-mediated lipoprotein oxidation was evaluated. C-PE (25 and 50 mg/kg body weight per d) was administered to experimental streptozotocin–nicotinamide-induced type 2 diabetic male rats for 28 d. C-PE treatment successfully ameliorated diabetic complications by decreasing food intake, organ weights, serum concentrations of glucose, cholesterol, TAG, VLDL-cholesterol, creatinine, uric acid and thiobarbituric acid-reactive substances (TBARS), with increases in body weight, Hb, total protein, bilirubin and ferric-reducing ability of plasma values. Hepatic and renal tissues demonstrated significant decreases in TBARS, lipid hydroperoxide and conjugated diene contents, with increases in superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, vitamin E and vitamin C levels. Furthermore, the 4-weekex vivoandin vitroadministration of C-PE (0·5 and 1·0 mg/ml) indicated a decrease in Cu-mediated serum oxidation. The kinetics of the LDL oxidation profile showed significant prolongation of the lag phase with declines in oxidation rate, conjugated dienes, lipid hydroperoxide and TBARS. Results indicated the involvement of C-PE in the amelioration of diabetic complications by significant reductions in oxidative stress and oxidised LDL-triggered atherogenesis.

scholarly journals A simple test for predisposition to LDL oxidation based on the fluorescence development during copper-catalyzed oxidative modification.

1991 ◽  
Vol 32 (2) ◽  
pp. 349-358
Author(s):  
L Cominacini ◽  
U Garbin ◽  
A Davoli ◽  
R Micciolo ◽  
O Bosello ◽  
...  
Keyword(s):  
Oxidative Modification ◽  
Ldl Oxidation ◽  
Simple Test

Correlations among Mucociliary Transport, Ciliary Function, and Ciliary Structure

1998 ◽  
Vol 12 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Mark Jorissen
Keyword(s):  
Defense Mechanisms ◽  
Ex Vivo ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Preliminary Evidence ◽  
Relevant Parameter ◽  
Mucociliary Transport ◽  
Ciliary Dyskinesia ◽  
Ciliary Beat

Mucociliary transport is one of the most important defense mechanisms of the airway. Mucociliary transport time or rate, as measured using the saccharin test or the radioisotope technique, respectively, is clinically the most relevant parameter, although subject to large intra- and interindividual variability. There is no correlation between mucociliary transport in vivo and ciliary beat frequency ex vivo. Preliminary evidence demonstrates that mucociliary transport correlates with ciliary structure and orientation as investigated with transmission and scanning electron microscopy. A correlation is presented between ciliary beat frequency and secondary ciliary abnormalities. This correlation can best be described according to the logistic sigmoid model (r = 0.69). Based on these functional data, an ultrastructural distinction is proposed among normal (less than 5%), light (5 to 15%), moderate (15 to 25%), and severe (more than 25%) secondary ciliary dyskinesia.

Abstract 177: Promotion Of Nitroso-redox Balance By Beta 3 Adrenoceptor Agonism: Therapeutic Implications For Cardiovascular Complications Of Diabetes

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Keyvan Karimi Galougahi ◽  
Chia-chi Liu ◽  
Alvaro Garcia ◽  
Natasha A Fry ◽  
Clare L Hawkins ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cardiac Myocytes ◽  
Vascular Dysfunction ◽  
Pump Current ◽  
Redox Balance ◽  
Cardiovascular Complications ◽  
Oxidative Modification ◽  
Oxidation Products ◽  
Therapeutic Implications ◽  
Endothelial Nitric Oxide

Rationale: Disrupted balance between NO and O2.- is central in pathobiology of diabetes-induced cardiomyopathy and vascular dysfunction. We examined if stimulation of β3 adrenergic receptors (β3 ARs), coupled to endothelial nitric oxide synthase (eNOS) activation, would re-establish NO/O2.- balance, relieve oxidative inhibition of key caveolar proteins and protect against diabetes-induced cardiovascular dysfunction. Methods/Results: A hyperglycemic, hyperinsulinemic state was established in male White New Zealand rabbits by infusion of the insulin receptor antagonist S961 (12 μg/kg/h). Diabetes induced NADPH oxidase-dependent glutathionylation (GSS-) of the caveolar proteins Na+-K+ pump’s β1 subunit and eNOS in cardiac myocytes and aorta, an oxidative modification that inhibits the pump and uncouples eNOS. Consistent with this, diabetes was associated with reduced electrogenic Na+-K+ pump current in voltage-clamped cardiac myocytes and impaired endothelium-dependent vasorelaxation. Selective β3 AR agonist CL316243 (CL, 40 μg/kg/h) restored NO levels analysed by spin-trapping of NO-Fe(DETC)2 complexes; decreased diabetes-induced elevation in O2.- measured by HPLC analysis of dihydroethidium oxidation products, improved endothelium-dependent vasorelaxation, and restored the Na+-K+ pump function in cardiac myocytes. These effects were mediated by CL abolishing diabetes-induced increase in eNOS-GSS and β1-GSS through a decrease in forward reaction rate for glutathionylation by suppressing diabetes-induced NADPH oxidase activation, which was further amplified by promotion of de-glutathionylation via enhancement in association of glutaredoxine-1, the enzyme catalysing de-glutathionylation, with eNOS and Na+-K+ pump. Conclusion: β3 AR activation re-established nitroso-redox balance and relieved oxidative inhibition of key caveolar proteins in diabetes. β3 AR agonists are promising in treatment of diabetes-induced cardiovascular complications.

scholarly journals The synergistic effect of daidzein and α-tocopherol or ascorbic acid on microsome and LDL oxidation

2010 ◽  
Vol 28 (No. 5) ◽  
pp. 385-391 ◽  
Author(s):  
H. Wang ◽  
M.W. Martin ◽  
S. Yin
Keyword(s):  
Ascorbic Acid ◽  
Antioxidant Properties ◽  
Liver Microsomes ◽  
Oxidative Modification ◽  
Alpha Tocopherol ◽  
Interactive Effects ◽  
Ldl Oxidation ◽  
Rat Liver Microsomes ◽  
Protective Effects ◽  
Potential Health

Isoflavone daidzein brings potential health benefits. Its antioxidant properties are considered to be responsible in part for its protective effects. We investigated the antioxidant effects of daidzein and its interactive effects with<br />&alpha;-tocopherol or ascorbic acid on Fe<sup>2+/</sup>ascorbate-induced oxidation of rat liver microsomes and copper-induced human low-density lipoprotein (LDL) oxidation. Although the inhibitory effect of daidzein on lipid peroxidation in microsome was weak, it effectively prevented LDL against oxidative modification by prolonging the lag time, decreasing the propagating rate, and suppressing malonaldehyde (MDA) and carbonyls formation. When daidzein was combined with &alpha;-tocopherol in microsomes oxidation and with ascorbic acid in LDL oxidation, the protection was significantly greater than the calculated additive effect of the two individual actions. Thus, daidzein can protect LDL from oxidative modification, and its combination with nutrients may be superior to the action of it alone. These results can help to get a better understanding of the interactions of different antioxidants in vivo.

scholarly journals Endothelial Glycocalyx Shedding Occurs during Ex Vivo Lung Perfusion: A Pilot Study

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Timothy M. Sladden ◽  
Stephanie Yerkovich ◽  
Douglas Wall ◽  
Maxine Tan ◽  
William Hunt ◽  
...  
Keyword(s):  
Ex Vivo ◽  
New Technology ◽  
Heparan Sulphate ◽  
Dynamic Compliance ◽  
Preliminary Evidence ◽  
Lung Perfusion ◽  
Endothelial Glycocalyx ◽  
Ex Vivo Lung Perfusion ◽  
Lung Dysfunction ◽  
Over Time

Background. Damage to the endothelium has been established as a key pathological process in lung transplantation and ex vivo lung perfusion (EVLP), a new technology that provides a platform for the assessment of injured donor lungs. Damage to the lung endothelial glycocalyx, a structure that lines the endothelium and is integral to vascular barrier function, has been associated with lung dysfunction. We hypothesised that endothelial glycocalyx shedding occurs during EVLP and aimed to establish a porcine model to investigate the mechanism underlying glycocalyx breakdown during EVLP. Methods. Concentrations of endothelial glycocalyx breakdown products, syndecan-1, hyaluronan, heparan sulphate, and CD44, were measured using the ELISA and matrix metalloproteinase (MMP) activity by zymography in the perfusate of both human (n = 9) and porcine (n = 4) lungs undergoing EVLP. Porcine lungs underwent prolonged EVLP (up to 12 hours) with perfusion and ventilation parameters recorded hourly. Results. During human EVLP, endothelial glycocalyx breakdown products in the perfusate increased over time. Increasing MMP-2 activity over time was positively correlated with levels of syndecan-1 (r = 0.886; p=0.03) and hyaluronan (r = 0.943; p=0.02). In the porcine EVLP model, hyaluronan was the only glycocalyx product detectable during EVLP (1 hr: 19 (13–84) vs 12 hr: 143 (109–264) ng/ml; p=0.13). Porcine hyaluronan was associated with MMP-9 activity (r = 0.83; p=0.02) and also with dynamic compliance (r = 0.57; p=0.03). Conclusion. Endothelial glycocalyx products accumulate during both porcine and human EVLP, and this accumulation parallels an accumulation of matrix-degrading enzyme activity. Preliminary evidence in our porcine EVLP model suggests that shedding may be related to organ function, thus warranting additional study.

PON1 arylesterase activity, HDL functionality and their correlation in malnourished children

2019 ◽  
Vol 32 (4) ◽  
pp. 321-326
Author(s):  
Mukund Ramchandra Mogarekar ◽  
Mahendrakumar Gajanan Dhabe ◽  
Mayuri Madhukarrao Palmate
Keyword(s):  
Lipid Profile ◽  
Lipid Hydroperoxide ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Paraoxonase 1 ◽  
Ldl Oxidation ◽  
Pon1 Activity ◽  
Phenyl Acetate ◽  
Malnourished Children ◽  
Hdl Functionality

Abstract Background The study was done to assess high-density lipoprotein (HDL) functionality and to correlate this with paraoxonase 1 (PON1) activity in malnourished children. It aimed to find the effect of malnutrition on changes in PON1 activity, HDL functionality, lipid profile and lipid hydroperoxide formation. Methods This case control study included 30 malnourished children (up to age 5 years) and 30 healthy controls in the paediatric inpatient department of SRTR Government Medical College Ambajogai, India. Clinically diagnosed cases depending on anthropometric indices were selected. Serum PON1 activity by using phenyl acetate as a substrate, HDL functionality by haemin by its protection on H2O2 and haemin induced LDL oxidation, lipid profile by routine enzymatic methods and lipid hydroperoxide using the FOX2 assay were measured. Results Malnourished children had significantly decreased PON1 activity (106.6 ± 12.74** vs. 132.23 ± 28.49 IU/L), HDL functionality (116.55 ± 8** vs. 132.29 ± 10.9%), total cholesterol (TC) (102.5 ± 16** vs. 116.4 ± 12.65 mg/dL), HDL-cholesterol (C) (33.41 ± 9.74** vs. 40.55 ± 5.85 mg/dL) and reduced total protein level (5.56 ± 0.91* vs. 6.06 ± 1.055) higher triglycerides (TG) (146.76 ± 34.97* vs. 125.96 ± 17.21 mg/dL) level and total hydroperoxide (TPX) levels (5.568 ± 1.70** vs. 3.22 ± 1.52 μM/L). *p < 0.05 **p < 0.001. PON1 activity (r2 = 0.576) and TC (r2 = 0.567) shows significant positive correlation with HDL functionality. PON1 activity, HDL-C, HDL functionality and TPX shows independent contribution towards malnutrition in children in multivariate and univariate logistic regression. TC lost its significance in multivariate regression. Conclusions Malnutrition leads to decrease in HDL functionality and increase in hydroperoxide levels with a decrease in PON1 activity.

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