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Plasma Glutathione (plasma + glutathione)
Selected AbstractsOpen-labeled pilot study of cysteine-rich whey protein isolate supplementation for nonalcoholic steatohepatitis patientsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2009Taned Chitapanarux Abstract Background and Aims:, Glutathione (GSH) depletion contributes to liver injury and development of steatohepatitis. Undenatured cysteine-rich whey protein isolate has been clinically proven to raise GSH in several patient groups. The aim of this study was to evaluate the effect of oral supplementation with whey protein on patients with nonalcoholic steatohepatitis (NASH). Methods:, In an open-labeled clinical trial, 38 patients (18 male, 20 female; mean age 48 ± 14 years) with NASH confirmed by computed tomography measurements and liver biochemistries were given with a daily dose of 20 g whey protein isolate for 12 weeks. Results:, A significant reduction in alanine aminotransferase (ALT) (64 ± 72 vs 46 ± 36, P = 0.016) and aspartate aminotransferase (AST) (45 ± 49 vs 33 ± 18, P = 0.047) were observed. Plasma glutathione and total antioxidant capacity increased significantly at the end of study (53 ± 11 vs 68 ± 11, P < 0.05 and 1.26 ± 0.10 vs 2.03 ± 0.10, P < 0.05). Liver attenuation index improved from ,13.4 ± 11.1 to ,9.7 ± 13.1 (P = 0.048). Hepatic macrovesicular steatosis decreased significantly after 12 weeks of supplementation (33.82 ± 12.82 vs 30.66 ± 15.96, P = 0.046). Whey protein isolate was well tolerated. No serious adverse events were observed. Conclusions:, The results indicate that oral supplementation of cysteine-rich whey protein isolate leads to improvements in liver biochemistries, increased plasma GSH, total antioxidant capacity and reduced hepatic macrovesicular steatosis in NASH patients. The results support the role of oxidative stress in the pathogenesis of this disease. [source] Glutathione depletion and cardiomyocyte apoptosis in viral myocarditisEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004V. Kytö Abstract Background, The course of viral myocarditis is highly variable. Oxidative stress and Bcl-2 family genes may play a role in its pathogenesis by regulating the amount of cardiomyocyte apoptosis. Apoptosis is difficult to detect and quantify in vivo. Therefore, we set to look for indicators of this potentially preventable form of cell death during various phases of experimental murine coxsackievirus B3 myocarditis. Methods, BALB/c mice were infected with the cardiotropic coxsackievirus B3 variant. Glutathione (HPLC), cardiomyocyte apoptosis (TUNEL and caspase-3 cleavage), Bax and Bcl-XL mRNA expression (real time RT-PCR), histopathology and viral replication (plaque assay and real time RT-PCR) were measured from day 3 to day 20 after infection. Results, Infection caused severe myocarditis and led to progressive decrease of plasma glutathione levels. Myocardial mRNA levels of pro-apoptotic Bax and antiapoptotic Bcl-XL were significantly increased from day 3 onwards. Bax mRNA and ratio of Bax to Bcl-XL correlated with cardiomyocyte apoptosis (r = 0·77, P = < 0·001 and r 0·51, P < 0·01, respectively). Cardiomyocyte apoptosis was highest on day 5, coinciding with a rapid decline in plasma glutathione (r = ,0·52, P = 0·003). Conclusions, Systemic oxidative stress as indicated by decreased plasma glutathione levels coincides with cardiomyocyte apoptosis in experimental coxsackievirus myocarditis. Decreased plasma glutathione levels and changes in cardiac Bax and Bcl-XL mRNA expression identify a phase of myocarditis in which the potentially preventable cardiomyocyte apoptosis is mostly observed. [source] Essential pathogenic and metabolic differences in steatosis induced by choline or methione-choline deficient diets in a rat modelJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2007Reeta Veteläinen Abstract Background and Aim:, Choline deficient (CD) and methione-choline deficient (MCD) diets are rodent models for steatosis, with potentially dissimilar biochemical backgrounds. The aim of this study was to assess the metabolic and pathological derangements in rats fed CD and MCD diets. Methods:, Male Wistar rats received CD or MCD diet up to 7 weeks. Nutritional status, liver histopathology, Kupffer cell-mediated inflammation and injury, oxidative stress via thiobarbituric reactive species (TBARS), hepatic and plasma glutathione (GSH) and insulin homeostasis were assessed. Results:, In CD-fed rats, mainly microvesicular steatosis developed with occasional inflammatory cells. In MCD-fed rats, macrovesicular steatosis progressed to steatohepatitis (collagen deposition, activated stellate cells). Hepatic TBARS was increased and GSH decreased in the MCD-fed rats compared to no changes in the CD-fed rats. The CD-fed rats developed obesity, dyslipidemia and insulin resistance, in contrast to undetectable plasma lipids, unaffected insulin homeostasis and loss of body weight in the MCD-fed rats. Conclusions:, The CD diet induced uncomplicated steatosis as compared to progressive inflammation and fibrinogenesis in the MCD diet. CD and MCD diets represent two pathogenically different models of steatosis. Although equivalence for the outcome of both diets can be found in clinical steatosis, the results of models using these diets should be compared with caution. [source] The Effect of Glutathione Modulation on the Concentration of Homocysteine in Plasma of RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2000Kjell K. Øvrebø Elevated plasma homocysteine concentration in humans is associated with increased risk of arteriosclerosis and ischaemic heart disease. We studied whether the plasma homocysteine concentration could be changed by administration of drugs that modulate the concentration of glutathione in both plasma and tissue. Male wistar rats received reduced glutathione (0.5 mmol/kg), N -acetylcysteine (0.5 mmol/kg), L-buthionine-[S,R]-sulfoximine (2 mmol/kg) or Ringer acetate intravenously. Twenty min. later an arterial blood sample was drawn for the measurement of homocysteine and other thiols in the plasma. The thiols were quantified by reversed-phase ion-pair liquid chromatography and fluorescence detection. The total homocysteine concentration in plasma of fasted rats was 6.1±0.5 ,M. Intravenous administration of reduced glutathione or N -acetylcysteine reduced the homocysteine concentration in plasma significantly by 51% to 3.0±0.3 ,M and 63% to 2.2±0.2 ,M, respectively (P<0.05). In contrast, L-buthionine-[S,R]-sulfoximine increased the concentration of homocysteine by 41% to 8.6±0.6 ,M (P<0.05). The glutathione concentration in plasma was 19.5±1.9 ,M in controls and was unchanged by N -acetylcysteine administration. Reduced glutathione increased plasma glutathione to 379.7±22.9 ,M (P<0.05), whereas L-buthionine-[S R]-sulfoximine lowered the plasma glutathione concentration to 5.3±0.4 ,M. Homocysteine was negatively correlated to the glutathione (r=,0.399, P<0.01) and the cysteine (r=,0.52, P<0.01) concentrations in plasma. Our conclusion is that modulation of the glutathione levels influences the concentration of homocysteine in plasma of rats. [source] | ||||||||||