Plasma thiols have been the object of growing interest because numerous
Arne lindgren 2 have indicated that even a mild degree of hyperhomocysteinemia is associated with an increased risk of developing occlusive vascular diseases 1 2 3 4 5. However, the mechanism behind the vascular injuries is still unknown. Studies of the possible pathogenetic mechanism of increased plasma homocysteine concentrations are difficult because little is known about mechanism for the formation of different homocysteine species in vivo.
We recently published a method that measures reduced and total fractions of homocysteine, cysteine, glutathione, and cysteinylglycine 6.
In a preliminary study, we found that patients suffering from stroke have hyperhomocysteinemia, whereas their reduced homocysteine was within the health-related reference interval 7. We hypothesized that the increased concentrations of the oxidized forms of homocysteine in plasma were attributable to a hyperoxidative state in the plasma. We also observed 8 that patients suffering from renal failure had concentrations of reduced homocysteine within the reference interval despite increased total homocysteine.
The redox state of homocysteine in plasma may be influenced by other thiols 9such as glutathione, which is involved in maintaining the intracellular thiols in reduced form. In the present "Arne lindgren 2," we therefore investigated the relationships between homocysteine, cysteine, and glutathione in 29 healthy subjects and 15 patients with renal or liver failure. We used a newly developed preparation procedure, especially designed to minimize several known pitfalls that frequently influence plasma glutathione determinations.
Increased hemolysis during sample collection causes falsely increased plasma "Arne lindgren 2" measurements because of the high glutathione contents in the blood cells. Furthermore, reduced glutathione disappears within minutes in cell-free plasma because of oxidation 7 10 11 In the present study, we also determined thiols in whole blood and hemoglobin in plasma.
Specimens were collected from nine anuric hemodialysis patients seven men and two women; mean age, 76 years; range, 55—79 years. No patient had clinical signs of heart failure or respiratory insufficiency, and there was no laboratory evidence Arne lindgren 2 liver dysfunction in any of the cases. The subjects received daily supplementation with 5 mg of folic acid and 5 mg of pyridoxine. Specimens were also collected from six male patients with liver disease mean age, 56 years; range, 28—74 years.
All of the patients had advanced liver disease with cirrhosis, one because of autoimmune hepatitis, and the others because of alcohol. None of the patients had pulmonary diseases or impaired renal function. Their ages did not differ significantly from the age of the patients with renal or liver failure.
Eight apparently healthy individuals participated in the comparison of the present method with the previously described method 6. Immediately within 10 s after sample collection, "Arne lindgren 2" tube was placed in ice and chilled for 6 min. The supernatant was applied to HPLC as described previously 6. The supernatant was used for the determination of reduced thiols as described previously 6. The Student independent t -test was used to test whether differences between the groups of patients and the healthy individuals were significant.
Linear regression analysis was used to obtain correlation coefficients. Plasma samples were mixed with the preparations 2 h after the sample collections and assayed the same day by HPLC.
Reported plasma concentrations in healthy subjects showed large variability, 0. Our modified preparation procedure improves the reliability of the method, and the values obtained for reduced and total thiols are similar to those that we 6 7 and others 17 have observed previously in healthy individuals. Both the decreased concentration of reduced plasma homocysteine and the increased concentration of total plasma homocysteine could be attributed to increased prooxidant activity in plasma from these Arne lindgren 2, which might lead to a rapid oxidation of reduced homocysteine to disulfides.
Homocysteine "Arne lindgren 2" to plasma proteins through disulfide bonds is not as metabolically available as homocysteine in low-molecular weight disulfides or in its reduced form and therefore accumulates in the circulation Another possible explanation for the decreased concentration of reduced plasma homocysteine is a lowered intracellular production of reduced homocysteine because of a more efficient metabolism of homocysteine caused by vitamin supplementation.
The total plasma homocysteine concentration was increased, whereas the concentrations of total glutathione and total cysteine in plasma were not significantly changed. The decreased whole blood concentration of reduced glutathione in this study and in others 28 29 might be attributable to lower hepatic production of glutathione in liver disease.
These findings show that glutathione does not influence the redox status of homocysteine or cysteine and suggest that glutathione is Arne lindgren 2 an exclusive reductant in plasma.
These findings suggest that reduced cysteine plays a role, at least partly, in the maintenance of the redox status in plasma. Skip to main content. View inline View popup. Whole blood concentration of reduced thiols. Homocysteine and cardiovascular disease [Review]. Annu Rev Medicine ; Plasma homocysteine as a risk factor for vascular disease.
The European Concerted Action Project. JAMA ; Hyperhomocysteinemia as a risk factor for arterial and venous disease. A review of evidence and relevance [Review]. Thromb Haemost ; Plasma homocyst e ine and arterial occlusive diseases. Clin Chem Low circulating folate and vitamin B 6 concentrations. Risk factors for stroke, peripheral vascular disease, and coronary artery disease. Circulation ; Homocysteine and other thiols determined in plasma by HPLC and thiol-specific postcolumn derivatization.
Effect of thiol oxidation and thiol export from erythrocytes on determination of redox status of homocysteine and other thiols in plasma from healthy subjects and patients with cerebral infarction. Reduced, free and total fractions of homocysteine and other thiol Arne lindgren 2 in plasma from patients with renal failure.
Nephron ; Reduced, oxidized and protein-bound forms of homocysteine and other aminothiols in plasma comprise the redox thiol status—a possible element of the extracellular antioxidant defense system. J Nutr ; Andersson MEMeister A. Dynamic state of glutathione in blood plasma. J Biol Chem ; Improved procedure for determining glutathione in plasma as an index of myocardial oxidative stress.
Determination of reduced, oxidized, and protein-bound glutathione in human plasma with precolumn derivatization with monobromobimane and liquid chromatography. Anal Biochem ; Plasma hemoglobin determination by recording derivative spectrophotometry.
Am J Clin Pathol ; High-dose intravenous glutathione in man. Pharmacokinetics and effects on cyst e ine Arne lindgren 2 plasma and urine. Eur J Arne lindgren 2 Investig ; Hyperhomocysteinemia induced by folic acid deficiency and methionine loading-applications of a modified HPLC method. Clin Chim Acta ; HPLC with o -phthaldialdehyde precolumn derivatization to measure total, oxidized, and protein-bound glutathione in blood, plasma, and tissue.
Determination of in vivo redox status of cysteine, cysteinylglycine, homocysteine and glutathione in human plasma. Anemia and chronic renal failure: Some pitfalls in the Arne lindgren 2 of blood glutathione. Clin Sci ; Wendel ACikryt P. The level and half-life of "Arne lindgren 2" in human plasma. FEBS Lett ; Blood and plasma glutathione measured in healthy subjects by HPLC: Glutathione antioxidant system as a marker of oxidative stress in chronic renal failure.
Free Radic Biol Med ; Plasma homocysteine and thiol compound fractions after oral administration of N -acetylcysteine. Scand J Clin Lab Investig ; Oxidative stress and antioxidant defense mechanism in glomerular diseases. Erythrocyte redox state in uremic anemia: Acta Haematol ; Redox state, antioxidative activity and lipid peroxidation in erythrocytes and plasma of chronic ambulatory peritoneal dialysis patients.
Effect of liver cirrhosis and age on the glutathione concentration in the plasma, erythrocytes, and gastric mucosa of man. Alteration of erythrocyte glutathione, cysteine and glutathione synthetase in alcoholic and non-alcoholic cirrhosis. Role of oxidative stress and antioxidant therapy in alcoholic and nonalcoholic liver diseases. Adv Pharmacol ; In this Vol. Table of Contents Index by author. Clinical Chemistry Jul45 7. Jump to section Article References.
Show more Technical Briefs. Arne Lindgren. Publication Preview. 3rd European Stroke Organisation Conference, Poster Abstracts European Stroke JournalVol. 2(IS) Object. Predictors of early (day) and long-term (1-year) mortality rates after primary intracerebral hemorrhage (ICH) were studied in a large population in.
Arne Lindgren. Neurology, Lund · Clinical Stroke. Genetic variation at 16q is associated with small vessel stroke · Traylor, Matthew; Malik, Rainer; Nalls.
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