Glutathione Levels In Patients Research Articles

The Ketogenic Diet Increases In Vivo Glutathione Levels in Patients with Epilepsy.

The Ketogenic Diet (KD) is a high-fat, low-carbohydrate diet that has been utilized as the first line treatment for contrasting intractable epilepsy. It is responsible for the presence of ketone bodies in blood, whose neuroprotective effect has been widely shown in recent years but remains unclear. Since glutathione (GSH) is implicated in oxidation-reduction reactions, our aim was to monitor the effects of KD on GSH brain levels by means of magnetic resonance spectroscopy (MRS). MRS was acquired from 16 KD patients and seven age-matched Healthy Controls (HC). We estimated metabolite concentrations with linear combination model (LCModel), assessing differences between KD and HC with t-test. Pearson was used to investigate GHS correlations with blood serum 3-B-Hydroxybutyrate (3HB) concentrations and with number of weekly epileptic seizures. The results have shown higher levels of brain GSH for KD patients (2.5 ± 0.5 mM) compared to HC (2.0 ± 0.5 mM). Both blood serum 3HB and number of seizures did not correlate with GSH concentration. The present study showed a significant increase in GSH in the brain of epileptic children treated with KD, reproducing for the first time in humans what was previously observed in animal studies. Our results may suggest a pivotal role of GSH in the antioxidant neuroprotective effect of KD in the human brain.

Effect of smokeless tobacco use on salivary glutathione levels among chronic periodontitis patients before and after non-surgical periodontal therapy.

INTRODUCTIONSmokeless tobacco (SLT) jeopardizes periodontal health and also produces an imbalance between reactive oxygen species (ROS) and antioxidants (AO) such as glutathione. Glutathione is an important redox regulator in saliva and its maintenance is essential for periodontal health. Periodontitis patients have a reduced total AO capacity in whole saliva, and periodontal therapy restores the redox balance. Hence, the purpose of this study was to investigate the effects of smokeless tobacco use on saliva glutathione levels in patients with chronic periodontitis and to evaluate these effects after non-surgical periodontal therapy.METHODSThe study included 100 subjects in four groups; healthy, gingivitis, and chronic periodontitis (CP) patients with and without SLT use. Saliva samples were collected, and clinical periodontal parameters were recorded at baseline and at one month after non-surgical periodontal therapy. Glutathione levels were analyzed using spectrophotometry at 412 nm. Statistical analysis was carried out using paired t-test, chi-squared, and analysis of variance (ANOVA).RESULTSMean glutathione values in saliva were found to be lower in periodontitis patients compared to SLT users at baseline and at 1 month post non-surgical periodontal therapy (p<0.001) In addition, non-surgical therapy leads to a highly significant improvement in the glutathione levels in gingivitis, in the CP with and without ST groups (p<0.001).CONCLUSIONSSuccessful non-surgical periodontal therapy leads to considerable progress in the redox balance, thus regulating glutathione levels and reducing the effects of SLT on the periodontium. This emphasises the importance of non-surgical therapy, especially among SLT users.

Glutathione, the Major Redox Regulator, in the Prefrontal Cortex of Individuals at Clinical High Risk for Psychosis.

IntroductionOxidative stress and glutathione dysregulation have been implicated in the etiology of schizophrenia. To date, most in vivo studies have investigated alterations in cerebral glutathione levels in patients in which the disorder is already established; however, whether oxidative stress actually predates the onset of psychosis remains unknown. In the current study, we investigated cerebral glutathione levels of antipsychotic-naïve individuals at clinical high risk for psychosis. As exploratory analyses, we also investigated the associations between cerebral glutathione levels and peripheral glutathione peroxidase activity and clinical and neuropsychological measures.MethodsGlutathione levels were measured in the medial prefrontal cortex of 30 clinical high risk (n=26 antipsychotic naïve) and 26 healthy volunteers using 3T proton magnetic resonance spectroscopy. Each participant was assessed for glutathione peroxidase activity in plasma and genotyped for the glutamate cysteine ligase catalytic subunit polymorphism.ResultsNo significant differences were observed in glutathione levels between clinical high risk and healthy volunteers in the medial prefrontal cortex (F(1,54)=0.001, P =0.98). There were no significant correlations between cerebral glutathione levels and clinical and neuropsychological measures. Similarly, no significant differences were found in peripheral glutathione peroxidase activity between clinical high risk and healthy volunteers (F(1,37)=0.15, P =0.70). However, in clinical high risk, we observed a significant effect of lifetime history of cannabis use on glutathione peroxidase activity (F(1,23)=7.41, P =0.01).DiscussionThe lack of significant differences between antipsychotic naïve clinical high risk and healthy volunteers suggests that alterations in glutathione levels in medial prefrontal cortex are not present in the clinical high risk state.

A Study of Effects of Addition of Coenzyme Q 10 to High Dose Statins in Patients of Coronary Artery Disease with Special Reference to Oxidative Balance

AbstractBackground: Oxidative stress is one of the most potent inductors of endothelial dysfunction and is involved at all stages of atherosclerotic plaque evolution. Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and are potent inhibitors of cholesterol biosynthesis. In clinical trials, statins are beneficial in the primary and secondary prevention of coronary heart disease. Statins also possess direct free radical scavenging activity. However, the prooxidant effect of statins has also been reported as statins block the mevalonate pathway and the synthesis coenzyme Q10. This Additional Coenzyme Q10 depletion by statins in patients with coronary artery disease (CAD) may be a critical issue as it may reduce absolute benefits of statins.Objectives: The purpose of this study was to investigate the effects of high dose statins on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in CAD patients who underwent recent PCI and to study whether addition of coenzyme Q10 (100 mg/d) has any additional effect on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in patients already receiving high dose statin therapy.Methods: Twenty-one consecutive patients who underwent percutaneous transluminal coronary angioplasty (PTCA) in Department of Cardiology at our institute were studied. The cases (n = 21) were given high dose statins for first 1 week and then coenzyme Q10 (100 md /day) is added for next 1 week. Plasma Malondialdehyde(MDA) levels and plasma glutathione levels were analyzed at the time of admission before giving statins and at the end of 1 week of statin therapy and again after 1 week of Co-Q therapy.Results: Our results indicate that a relation exists between high plasma Malondialdehyde (MDA) levels and low plasma glutathione levels with coronary artery disease. High dose statins decrease MDA levels and increase plasma glutathione levels, even though they decrease coenzyme q levels in the body. It was also shown that addition of Coenzyme Q10 at 100 mg/d enhances plasma glutathione levels and decreases plasma MDA level still further in patients who have CAD, already receiving high dose statin therapy.Conclusions: Addition of Coenzyme Q10 at 100 mg/d has an additive effect with high dose statins in decreasing oxidative stress. Particularly in light of the excellent tolerance and affordability of this natural physiological compound, supplemental Coenzyme Q10 may emerge as an attractive option in future, and merits evaluation in additional large studies.

Lipid Peroxidation Product and Glutathione Levels in Patients with Coronary Heart Disease Before and After Surgery

Background: It has been reported that ischemia-reperfusion is associated with augmentation of oxidative stress and its specific and sensitive markers. Oxidative stress may cause atrial fibrillation (AF) which is a common consequence after cardiac surgery. Dietary supplementation with antioxidants might lower the incidence of AF following coronary artery bypass graft (CABG) surgery. Materials and Methods: Fifty patients with coronary heart disease (CHD) referred to Namazi and Faghihi Hospitals in Shiraz, undergone elective CABG, were enrolled in this study. For evaluation of oxidative stress, whole blood was taken before and 24 hours after surgery and malondialdehyde (MDA) as an oxidative marker and glutathione (GSH) as an antioxidant marker were measured. Results: Results showed a significant difference between the mean concentration of GSH before and after CABG surgery (P &lt;0.05); however, the difference in plasma MDA levels before and after CABG was insignificant. Conclusion: CABG surgery results in oxidative stress and reduces GSH 24h after surgery and administration of antioxidants may attenuate post-operative oxidative stress. [GMJ.2015;4(2):78-82]

2699 – Glutathione levels in patients with chronic and fist-episode schizophrenia and association with neurological soft signs

Introduction Recent studies have suggested that the deficit of glutathione (GSH), a major antioxidant, seems to play a role in the pathophysiology of schizophrenia. Moreover, oxidative stress may contribute to the development of neurological abnormalities, including tardive dyskinesia and parkinsonism symptoms. Objectives To determine plasma glutathione levels and to explore their association with neurological soft signs (NSS) in patients with chronic and first-episode schizophrenia. Methods A case-control study carried-out on three groups: sixty clinically stable patients with chronic schizophrenia, twentythree patients with first-episode schizophrenia and thirty matched healthy controls. Glutathione levels: total (GSHt), reduced (GSHr) and oxidized glutathione (GSSG) were determined by spectrophotometry. NSS were assessed in three groups by a standardized neurological examination (Krebs et al., 2000). Results Plasmatic GSHt and GSHr levels were significantly decreased in patients with chronic and first-episode schizophrenia. All NSS scores were significantly higher in two groups of patients compared to controls. No association was found between NSS scores and glutathione levels in patients with chronic schizophrenia. However, in patients with firstepisode, a negative correlation was found between GSHt levels and involuntary movement sub-score (r= -0.62, p=0.008). Conclusion These results suggest that GSH deficit is not related to the stage of disease and may be an important indirect biomarker of oxidative stress in schizophrenia. The association between low GSHt level as a marker of oxidative stress and involuntary movements could suggest that oxidative stress may contribute to the brain damage which leads to an increased prevalence of these NSS.

2700 – Glutathione levels and schizotypy scores in unaffected first-degree relatives of patients with schizophrenia

Several studies have shown a glutathione (GSH) deficit in patients with schizophrenia. It may in part arise from a genetically compromised synthesis of GSH, the major cellular antioxidant and redox-regulator. First-degree relatives of patients with schizophrenia share many susceptibility genes of this disease. The objectives of this study were to determine plasma glutathione levels in patients with schizophrenia and their unaffected first-degree relatives of compared to healthy controls and to examine the correlation between glutathione levels and schizotypy scores in unaffected relatives. We included 60 patients with schizophrenia, 33 of their unaffected siblings and 30 healthy controls with no family psychiatric history. The blood glutathione levels: total (GSHt), reduced (GSHr), and oxidized glutathione (GSSG) were measured by spectrophotometry. Schizotypy scores were assessed by the schizotypal personality questionnaire (SPQ). GSHt and GSHr were significantly lower in patients than in controls, whereas there was no difference in glutathione levels between unaffected relatives and healthy controls. Moreover, no correlation was found between glutathione levels and schizotypy scores in unaffected relatives of patients with schizophrenia. These results reveal that unaffected relatives of patients with schizophrenia didn’t have a GSH deficit. In the same group, no correlation was found between glutathione levels and schizotypy scores which considered a vulnerability marker for schizophrenia. These findings disagree with our hypothesis that GSH deficit could be a biological marker of vulnerability to schizophrenia. However, further studies are necessary to explore this hypothesis.

Dietary Supplementation with Pressurized Whey in Patients with Cystic Fibrosis

Cystic fibrosis (CF) is characterized by malnutrition, chronic pulmonary inflammation, and oxidative stress. Whey protein is rich in sulfhydryl groups and is recognized for its ability to increase glutathione and reduce oxidative stress. Previously, we have shown that supplementation with whey increased intracellular glutathione levels in patients with CF. We have subsequently shown that hyperbaric pressure treatment of whey protein promotes the release of novel peptides for absorption, increases intracellular glutathione in healthy subjects, and reduces in vitro production of interleukin (IL)-8. We hypothesized that pressurized whey supplementation in children and adults with CF could have significant nutritional and anti-inflammatory benefits. A pilot open-label study of 1-month dietary supplementation with pressurized whey in CF patients was undertaken to assess the effects. Twenty-seven patients with CF (nine children, 18 adults) were enrolled. The dose of pressurized whey was 20 g/day in patients less than 18 years of age and 40 g/day in older patients. Anthropometric measures, pulmonary function, serum C-reactive protein (CRP), whole blood glutathione, and whole blood IL-8 and IL-6 responses to phytohemagglutinin (PHA) stimulation were measured at baseline and at 1 month. Three adults withdrew (one with gastrointestinal side effects, two with acute infection). Both children and adults showed enhancements in nutritional status, as assessed by body mass index. Children showed improvement in lung function (forced expiratory volume in 1 second). The majority of patients with an initially elevated CRP showed a decrease. PHA-stimulated IL-8 responses tended to decrease in the adults. Whole blood glutathione levels did not change. Thus, oral supplementation with pressurized whey improves nutritional status and can have additional beneficial effects on inflammation in patients with CF.

Mechanistic Details of Glutathione Biosynthesis Revealed by Crystal Structures of Saccharomyces cerevisiae Glutamate Cysteine Ligase

Glutathione is a thiol-disulfide exchange peptide critical for buffering oxidative or chemical stress, and an essential cofactor in several biosynthesis and detoxification pathways. The rate-limiting step in its de novo biosynthesis is catalyzed by glutamate cysteine ligase, a broadly expressed enzyme for which limited structural information is available in higher eukaryotic species. Structural data are critical to the understanding of clinical glutathione deficiency, as well as rational design of enzyme modulators that could impact human disease progression. Here, we have determined the structures of Saccharomyces cerevisiae glutamate cysteine ligase (ScGCL) in the presence of glutamate and MgCl(2) (2.1 A; R = 18.2%, R(free) = 21.9%), and in complex with glutamate, MgCl(2), and ADP (2.7 A; R = 19.0%, R(free) = 24.2%). Inspection of these structures reveals an unusual binding pocket for the alpha-carboxylate of the glutamate substrate and an ATP-independent Mg(2+) coordination site, clarifying the Mg(2+) dependence of the enzymatic reaction. The ScGCL structures were further used to generate a credible homology model of the catalytic subunit of human glutamate cysteine ligase (hGCLC). Examination of the hGCLC model suggests that post-translational modifications of cysteine residues may be involved in the regulation of enzymatic activity, and elucidates the molecular basis of glutathione deficiency associated with patient hGCLC mutations.

Glutathione Deficiency in Cardiac Patients Is Related to the Functional Status and Structural Cardiac Abnormalities

BackgroundThe tripeptide glutathione (L-gamma-glutamyl-cysteinyl-glycine) is essential to cell survival, and deficiency in cardiac and systemic glutathione relates to heart failure progression and cardiac remodelling in animal models. Accordingly, we investigated cardiac and blood glutathione levels in patients of different functional classes and with different structural heart diseases.MethodsGlutathione was measured using standard enzymatic recycling method in venous blood samples obtained from 91 individuals, including 15 healthy volunteers and 76 patients of New York Heart Association (NYHA) functional class I to IV, undergoing cardiac surgery for coronary artery disease, aortic stenosis or terminal cardiomyopathy. Glutathione was also quantified in right atrial appendages obtained at the time of surgery.ResultsIn atrial tissue, glutathione was severely depleted (−58%) in NYHA class IV patients compared to NYHA class I patients (P = 0.002). In patients with coronary artery disease, this depletion was related to the severity of left ventricular dysfunction (P = 0.006). Compared to healthy controls, blood glutathione was decreased by 21% in NYHA class I patients with structural cardiac disease (P<0.01), and by 40% in symptomatic patients of NYHA class II to IV (P<0.0001). According to the functional NYHA class, significant depletion in blood glutathione occurred before detectable elevation in blood sTNFR1, a marker of symptomatic heart failure severity, as shown by the exponential relationship between these two parameters in the whole cohort of patients (r = 0.88).ConclusionsThis study provides evidence that cardiac and systemic glutathione deficiency is related to the functional status and structural cardiac abnormalities of patients with cardiac diseases. These data also suggest that blood glutathione test may be an interesting new biomarker to detect asymptomatic patients with structural cardiac abnormalities.

Glutathione levels in patients with erectile dysfunction, with or without diabetes mellitus

The reduced form of glutathione (GSH) is the most important cell antioxidant and is also an essential cofactor for nitric oxide (NO) synthase that synthesizes NO from l-arginine. Reduced levels of GSH, due both to a hyperglycaemia-induced increase of free radical production and to a decrease of NADPH levels [like in diabetes mellitus (DM)], can hamper the endothelial cell functions. This condition may play an important role in the aetiology of some clinical signs, like erectile dysfunction (ED). The aim of this study was to test the hypothesis that GSH concentration is reduced in patients with ED and type 2 diabetes mellitus. We studied 111 male patients with ED: 64 with diabetes (ED/DM) and 47 without diabetes (ED/wDM); 20 patients with diabetes but without ED (DM) and 26 male normal subjects as a control group (C). The GSH red blood cell concentration was significantly lower in ED than in C (X +/- SD; 1782.12 +/- 518.02 vs. 2269.20 +/- 231.56 mumol/L, p < 0.001). In particular, GSH was significantly reduced in ED/DM vs. ED/wDM (1670.74 +/- 437.68 vs. 1930.63 +/- 581.01 micromol/L, p < 0.01). In DM, GSH was significantly lower than in C and significantly higher than in ED/DM (2084.20 +/- 118.14 vs. 2269.20 +/- 231.56 and vs. 1670.74 +/- 437.68 micromol/L, p < 0.002 and p < 0.001 respectively). GSH showed a negative correlation with fasting glucose concentrations (r = -0.34, p < 0.01) and with the duration of DM (r = -0.25, p < 0.05). A GSH depletion can lead to a reduction of NO synthesis, thus impairing vasodilation in the corpora cavernosa.

Lipid peroxidation, vitamins C, E and reduced glutathione levels in patients with pulmonary tuberculosis.

The present study examined the relationship between lipid peroxidation and vitamin C, vitamin E and reduced glutathione levels in plasma, erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients and an equal number of age-and sex-matched healthy subjects. Enhanced plasma, erythrocytes and erythrocyte membrane lipid peroxidation with concomitant decline in vitamin C, vitamin E and reduced glutathione levels were found in pulmonary tuberculosis patients. The elevated lipid peroxidation and decreased vitamin C, vitamin E and reduced glutathione levels indicate the potential of oxidative damage to erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients.

Alzheimer’s disease and total plasma aminothiols

Background Plasma homocysteine is elevated in Alzheimer’s disease, but little is known regarding levels of related aminothiols in the disease. We therefore determined total plasma homocysteine, cysteine, and glutathione levels in patients and control subjects and investigated their relationship with cognitive scores. Methods We performed a prospective, case-controlled survey based in two UK Psychogeriatric Assessment Centres. Fifty patients with features compatible with DSM-IV criteria for primary degenerative dementia of Alzheimer type were recruited together with 57 cognitively intact age- and gender-matched control subjects. Mini-Mental State and Alzheimer’s Disease Assessment Scale–Cognitive Subsection (ADAS-Cog) scores were determined for patients and control subjects. Aminothiols were assayed with an automated high-performance liquid chromatography (HPLC) system. Results Patients had significantly elevated total plasma homocysteine ( p < .001) and cysteine ( p < .01), but there were no group differences for total plasma glutathione. Glutathione was, however, a highly significant and independent predictor of cognitive scores in patients ( p = .002); lower plasma levels were associated with more severe cognitive impairment. Conclusions Total plasma homocysteine and cysteine are elevated in Alzheimer’s disease, suggesting intact transsulphuration but defective remethylation of homocysteine in the disease. Total plasma glutathione levels in patients correlate with cognitive scores. Taken together, these observations perhaps reflect the differential effects of Alzheimer’s disease–related oxidative stress on the two key pathways of homocysteine metabolism.

Brain glutathione levels in patients with epilepsy measured by in vivo (1)H-MRS.

Glutathione in its reduced form (GSH) is the most important free radical scavenging compound in the mammalian nervous system that prevents membrane lipid peroxidation. It is suspected that epileptic seizures are accompanied by a massive production of reactive oxygen species, i.e., oxidative stress. Using an (1)H MRS technique developed at the authors' site, the authors measured glutathione levels in a volume of interest (VOI) of 25 x 25 x 25 mm placed in structurally normal-appearing tissue in the parietooccipital region of each hemispheres in patients with and without active epilepsy, and in a age-matched control group. The GSH/water ratio in patients with epilepsy was significantly reduced in the parietooccipital region of both hemispheres (1.6 +/- 1.0 x 10(-5)) compared to the GSH/water ratio in healthy controls (2.4 +/- 1.1 x 10(-5)). There was no significant difference between the hemisphere with epileptogenic focus and the hemisphere without epileptogenic focus. The GSH/water ratios of the patients without active epilepsy were not different from the GSH/water ratios of patients with active epilepsy. The authors found evidence for a widespread impairment of the glutathione system in patients with epilepsy independent from seizure activity.

Superoxide Anion Formation and Glutathione Levels in Patients with Preeclampsia

Increased free radical activity has been implicated in the pathogenesis of preeclampsia. This article investigates the glutathione status in preeclampsia and whether superoxide generation is enhanced in preeclampsia. Venous blood samples were obtained from 30 preeclamptic women and 30 normotensive pregnant women (controls). Superoxide generation and glutathione content were measured. There was a significant increase in superoxide generation and a marked reduction in glutathione content in preeclamptic women as compared to controls (p < 0.001). These results indicate that enhanced superoxide generation and impaired glutathione metabolism may be involved in the pathogenesis of preeclampsia.

Oxidants/antioxidants in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is characterized by an increased oxidant burden and by a deficiency of glutathione, a major antioxidant, in the lung epithelial lining fluid (ELF). Therefore, a rational therapeutic approach is to reverse the imbalance between oxidants and antioxidants in the lung by enhancing the antioxidant screen. With this background, the aim of our study was to evaluate oral N-acetylcysteine (NAC) as a strategy to augment lung glutathione levels in patients with IPF Concentrations of total glutathione in bronchoalveolar lavage fluid (BALF) were quantified spectrophotometrically, before and following oral therapy with 3 x 600 mg NAC per day for 5 days, in 17 nonsmoking patients with biopsy-proven IPF. The volume of ELF recovered by BAL was determined using the urea method. Pretherapy, total glutathione levels in ELF in IPF patients were significantly less than normal (187 ± 36 vs 368 ± 60 μM), in contrast to levels in BALF (0.99 ± 0.12 vs 1.18 ± 19 μM). Following therapy with oral NAC, glutathione levels in BALF were 1.54 ± 0.24 μM (a significant increase compared to pretherapy), whereas the increase in ELF levels (319 ± 92 μM) did not reach significance. The therapy was well-tolerated, and all routine clinical and bronchoscopic parameters remained unchanged. It is thus feasible and safe to augment deficient lung glutathione levels in patients with IPF ; thereby, potentially augmenting pulmonary antioxidant protection. (Eur Respir J 1994 ;7 :431-6)

The effect of oral N-acetylcysteine on lung glutathione levels in idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is characterized by an increased oxidant burden and by a deficiency of glutathione, a major antioxidant, in the lung epithelial lining fluid (ELF). Therefore, a rational therapeutic approach is to reverse the imbalance between oxidants and antioxidants in the lung by enhancing the antioxidant screen. With this background, the aim of our study was to evaluate oral N-acetylcysteine (NAC) as a strategy to augment lung glutathione levels in patients with IPF. Concentrations of total glutathione in bronchoalveolar lavage fluid (BALF) were quantified spectrophotometrically, before and following oral therapy with 3 x 600 mg NAC per day for 5 days, in 17 nonsmoking patients with biopsy-proven IPF. The volume of ELF recovered by BAL was determined using the urea method. Pretherapy, total glutathione levels in ELF in IPF patients were significantly less than normal (187 +/- 36 vs 368 +/- 60 microM), in contrast to levels in BALF (0.99 +/- 0.12 vs 1.18 +/- 0.19 microM). Following therapy with oral NAC, glutathione levels in BALF were 1.54 +/- 0.24 microM (a significant increase compared to pretherapy), whereas the increase in ELF levels (319 +/- 92 microM) did not reach significance. The therapy was well-tolerated, and all routine clinical and bronchoscopic parameters remained unchanged. It is thus feasible and safe to augment deficient lung glutathione levels in patients with IPF; thereby, potentially augmenting pulmonary antioxidant protection.

Erythrocyte and plasma glutathione levels in patients with chronic renal insufficiency.

Reduced glutathione (GSH) levels were investigated in the erythrocytes and plasma of nondialyzed patients with varying degrees of renal insufficiency and also of patients on regular hemodialysis treatment. GSH levels were from 19 to 70% higher in the erythrocytes of examined patients as compared to their corresponding age-matched controls. A correlation was found between the degree of renal insufficiency and the erythrocyte GSH level. No variations in plasma GSH levels which could be related to the degree of renal deterioration were observed. A routine hemodialysis did not significantly affect erythrocyte and plasma GSH levels. No significant differences in GSH levels between anemic and nonanemic uremic patients were observed.

Hepatic glutathione content in patients with alcoholic and non alcoholic liver diseases

Reduced and oxidized hepatic glutathione was evaluated during alcoholic and non alcoholic liver injury. We studied 35 chronic alcoholics, 20 patients with non alcoholic liver diseases, 15 control subjects. Hepatic glutathione was measured in liver biopsies and correlated with histology and laboratory tests. Alcoholic and non alcoholic patients exhibited a significant decrease of hepatic glutathione compared to control subjects (controls: 4.14 ± 0.1 μmol/g liver; alcoholics: 2.55 ± 0.1, p<0.001; non alcoholics 2.77 ± 0.1, p<0.001). Oxidized glutathione was significantly higher in the two groups of patients compared to controls (controls: 4.4 ± 0.2% of total ; alcoholics 8.2 ± 0.3, p<0.001; non alcoholics: 8.5 ± 0.8, p<0.001). The decreased hepatic glutathione levels in patients with alcoholic and non alcoholic liver diseases may represent a contributing factor of liver injury and may enhance the risk of toxicity in these patients.

Effect of halothane and enflurane anaesthesia on the level of reduced glutathione in human red blood cells.

No significant changes were found in packed cell volume, haemoglobin concentration and red cell glutathione levels in patients before and after anaesthesia with halothane or enflurane. These results, though unable to explain the mechanism, support the earlier suggestion that glutathione plays little, if any, role in protecting liver against toxic effects of these anaesthetic agents or their metabolites.