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      Oxidizability assay of unfractionated plasma of patients’ with different plasma profile: a methodological study

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          Abstract

          Background

          Present study describe the in vitro model of plasma oxidation of patients with different lipid profile, that can be correlated to their invivo plasma oxidizability in order to find the arterial diseases prone patient groups.

          Method

          The method applied here to measure the invitro plasma oxidizability, accounts a convenient way that can be well suited in any clinical laboratory settings. Un-fractionated plasma was exposed to CuSO4 (5.0 mmol/L), a pro-oxidant, and low frequency ultrasonic wave to induce oxidation, and finally oxidizability was calculated by TBARS and Conjugated Diene methods.

          Result

          In our study, plasma LDL greater than 150 mg/dL possess 1.75 times more risk to undergo oxidation (CI, 0.7774 to 3.94; p = 0.071) than the low LDL plasma, percent of oxidation increased from 38.3% to 67.1% for the LDL level upto 150 mg/dL and high. Lag phase, which is considered as the plasma antioxidative protection, was also influenced by the higher LDL concentration. The mean lag time was 65.27 ± 20.02 (p = 0.02 compared to healthy), where as for 94.71 ± 35.11 min for the normolipidemic subject. The plasma oxidizability was also changed drastically for total cholesterol level, oxidative susceptibility shown 35% and 55.02% for 200 mg/dL and high respectively, however it didn’t appear as risk factor. Patient samples were also stratified according to their age, gender, and blood glucose level. Older persons (≥40 years) were 1.096 times (95% CL, 0.5607 to 2.141, p = 0.396) than younger (≤39 years age), males are 1.071 (95% CI, 0.5072- 2.264) times than the females, and diabetic patients are 1.091 (CI, 0.6153 to 1.934, p = 0.391) times in more risk than the non-diabetic counterpart.

          Conclusion

          This method addressing its easy applicability in biomedical research. And by this we were able to show that patients with high LDL (≥150 mg/dL) are in alarming condition besides diabetic and elderly (≥40 years age) males are considered to be susceptible and more prone to develop vascular diseases.

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          Most cited references26

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          Low density lipoprotein oxidation and its pathobiological significance.

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            Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT).

            The 356,222 men aged 35 to 57 years, who were free of a history of hospitalization for myocardial infarction, screened by the Multiple Risk Factor Intervention Trial (MRFIT) in its recruitment effort, constitute the largest cohort with standardized serum cholesterol measurements and long-term mortality follow-up. For each five-year age group, the relationship between serum cholesterol and coronary heart disease (CHD) death rate was continuous, graded, and strong. For the entire group aged 35 to 57 years at entry, the age-adjusted risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220, 221 to 244, and greater than or equal to 245 mg/dL [4.71 to 5.22, 5.25 to 5.69, 5.72 to 6.31, and greater than or equal to 6.34 mmol/L]) relative to the lowest quintile were 1.29, 1.73, 2.21, and 3.42. Of all CHD deaths, 46% were estimated to be excess deaths attributable to serum cholesterol levels 180 mg/dL or greater (greater than or equal to 4.65 mmol/L), with almost half the excess deaths in serum cholesterol quintiles 2 through 4. The pattern of a continuous, graded, strong relationship between serum cholesterol and six-year age-adjusted CHD death rate prevailed for nonhypertensive nonsmokers, nonhypertensive smokers, hypertensive nonsmokers, and hypertensive smokers. These data of high precision show that the relationship between serum cholesterol and CHD is not a threshold one, with increased risk confined to the two highest quintiles, but rather is a continuously graded one that powerfully affects risk for the great majority of middle-aged American men.
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              The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease.

              Anon. (1984)
              The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), a multicenter, randomized, double-blind study, tested the efficacy of cholesterol lowering in reducing risk of coronary heart disease (CHD) in 3,806 asymptomatic middle-aged men with primary hypercholesterolemia (type II hyperlipoproteinemia). The treatment group received the bile acid sequestrant cholestyramine resin and the control group received a placebo for an average of 7.4 years. Both groups followed a moderate cholesterol-lowering diet. The cholestyramine group experienced average plasma total and low-density lipoprotein cholesterol (LDL-C) reductions of 13.4% and 20.3%, respectively, which were 8.5% and 12.6% greater reductions than those obtained in the placebo group. The cholestyramine group experienced a 19% reduction in risk (p less than .05) of the primary end point--definite CHD death and/or definite nonfatal myocardial infarction--reflecting a 24% reduction in definite CHD death and a 19% reduction in nonfatal myocardial infarction. The cumulative seven-year incidence of the primary end point was 7% in the cholestyramine group v 8.6% in the placebo group. In addition, the incidence rates for new positive exercise tests, angina, and coronary bypass surgery were reduced by 25%, 20%, and 21%, respectively, in the cholestyramine group. The risk of death from all causes was only slightly and not significantly reduced in the cholestyramine group. The magnitude of this decrease (7%) was less than for CHD end points because of a greater number of violent and accidental deaths in the cholestyramine group. The LRC-CPPT findings show that reducing total cholesterol by lowering LDL-C levels can diminish the incidence of CHD morbidity and mortality in men at high risk for CHD because of raised LDL-C levels. This clinical trial provides strong evidence for a causal role for these lipids in the pathogenesis of CHD.
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                Author and article information

                Contributors
                Journal
                J Diabetes Metab Disord
                J Diabetes Metab Disord
                Journal of Diabetes and Metabolic Disorders
                BioMed Central
                2251-6581
                2014
                1 May 2014
                : 13
                : 54
                Affiliations
                [1 ]Department of Pharmacy, Primeasia University, 9 Banani C/A, Dhaka 1213, Bangladesh
                [2 ]Exim Bank Hospital, 840 Rokeya Soroni, Mirpur, Dhaka 1216, Bangladesh
                [3 ]Clinical Investigation Centre, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
                Article
                2251-6581-13-54
                10.1186/2251-6581-13-54
                4031925
                f4d1f71f-3422-4330-8779-48a5483f19f7
                Copyright © 2014 Imam et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 16 November 2013
                : 10 April 2014
                Categories
                Research Article

                plasma oxidation,conjugated diene,tbars,type ii diabetes

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