The relations of circulating agouti-related peptide and leptin with altered sleep architecture in patients with active Cushing's disease: a pilot study.

AIM: To evaluate sleep architecture of patients with Cushing's disease (CD) and to explore whether agouti-related peptide (AgRP) and/or leptin play a permissive role in sleep alterations in patients with active CD. METHODS: We performed polysomnography on 26 patients with active CD and age 26 age- and sex-matched control subjects. Blood samples were obtained from all participants for the analyzes of AgRP and leptin. The laboratory and sleep-related parameters were compared. RESULTS: The groups were similar in age, gender, and body mass index. The CD group had reduced sleep efficiency (71.6 ± 12.1% vs. 78.8 ± 12.6%, p = 0.042) and increased wake after sleep onset (WASO%) (24.7 ± 13.1% vs. 17.4 ± 11.6%, p = 0.040) as compared to control group. Seventeen patients with CD (65.4%) and 18 control subjects (69.2%) had obstructive sleep apnea. Serum AgRP (13.2 ± 7.4 pg/ml vs. 9 ± 3.1, p = 0.029), leptin (59.5 mcg/l, [IQR] 32.6-94.6 vs. 25.3 mcg/l, [IQR] 12.9-57.5, p = 0.007) were higher in CD group. AgRP and leptin correlated negatively with total sleep time, sleep efficiency, stage N2 sleep (%), and positively with WASO%. In multiple regression analyses, serum cortisol (ß = - 0.359, p = 0.042) and AgRP (ß = - 0.481, p = 0.01) were significant predictor of sleep efficiency. AgRP was also significant predictor of WASO% (ß = 0.452 and p < 0.05). CONCLUSIONS: Active CD carries an increased risk of impaired sleep efficiency and continuity which may worsen health-related quality of life. Elevated circulating AgRP and, to a lesser extent, leptin may be associated with decreased sleep efficiency and continuity in patients with CD. Patients with CD who have subjective sleep symptoms should be screened with polysomnography.

The utility of TNF-α, IL-6 and IL-10 in the diagnosis and/or follow-up food allergy.

BACKGROUND: Several pro-inflammatory and anti-inflammatory mediators play a role in the immunopathogenesis of food allergy (FA). The aim of this study was to investigate the utility of serum biomarkers like interleukin (IL)-10, TNF-α, and IL-6 in the diagnosis and/or follow-up of FA. METHODS: Sixty (25 females, 41.6%) newly diagnosed FA patients [IgE mediated (group-1, n=37), non-IgE (group-2, n=23)] with a median age of nine (1-33) months were enrolled. Twenty-four healthy children with a median age of eight (1-36) months constituted the control group (CG). In all the subjects, serum TNF-α, IL-6 and IL-10 levels were evaluated at the time of diagnosis and reassessed four weeks after therapeutic elimination diet (TED). RESULTS: The mean white blood cell count and median absolute eosinophile count of the CG were significantly lower than group-1 (p values were 0.019 and 0.006, respectively). The mean absolute neutrophile count and the median IL-6 were significantly higher in group-1 when compared with group-2 (p values were 0.005 and 0.032, respectively. Median TNF-α and IL-6 levels were significantly higher in the pre-TED among all patients (p values were 0.005 and 0.018, respectively). In group-1, median TNF-α and IL-6 levels decreased significantly after TED (p values were 0.01 and 0.029, respectively). CONCLUSIONS: Our findings support the role of inflammation in the pathogenesis of FA. Serum TNF-α and IL-6 levels may be useful markers for follow-up in FA, especially among IgE-mediated FA patients. Evaluation of IL-10 results was not sufficient for an interpretation of clinical tolerance.

The relationship between carotid intima-media thickness and serum secreted frizzled-related protein-4 and dipeptidyl peptidase-4 in diabetic patients with cardiovascular diseases.

We investigated the association between carotid intima-media thickness (CIMT) with clusterin (CLU), amylin, secreted frizzled-related protein-4 (SFRP-4), glucagon-like peptide-1 (GLP-1) levels, and dipeptidyl peptidase-4 (DPP-4) in type 2 diabetes mellitus (T2DM) individuals with or without coronary artery disease (CAD). This study consisted of four groups: control group (mean ages: 50.3±10.7 years; 20 females and 15 males), diabetic group (DM; mean ages: 53.9±11.1; 14 females and 23 males), CAD group (mean ages: 60.1±43.5; 17 females and 17 males) and CAD+DM group (mean ages: 62.6±11.8 years; 18 females and 18 males). CIMT levels in both CAD and CAD+DM groups are higher than those in controls. CIMT levels in CAD+DM group are also significantly higher than those in DM group. Left external carotid artery (ECA) was found different from controls only in DM group. The levels of SFRP-4 in control group were significantly lower than those in DM, CAD and CAD+DM groups. Serum GLP-1total levels were found to be significantly low in CAD+DM group when compared to control group. DPP-4 and SFRP-4 levels may be a predictive marker for atherosclerosis in diabetes while particularly in diabetes, they correlate well with HOMA-IR. CIMT has the potential to be a clinically useful predictor of vascular risk in diabetic patients with CAD (Tab. 3, Fig. 2, Ref. 39). Keywords: type 2 diabetes mellitus, carotid intima-media thickness, glucagon-like peptide-1, dipeptidyl peptidase-4, clusterin, amylin, secreted frizzled-related protein-4.

The relationship between IGF-2, IGFBP-2, and IGFBP-3 levels in patients suffering from pre-diabetes.

Many studies have shown that intervention in the early stages of diabetes may have a pivotal role in reducing the risk of cardiovascular diseases. This study was designed to assess possible relationships between insulin-like growth factor 2 (IGF-2), insulin-like growth factor binding proteins 2 and 3 (IGFBP-2, IGFBP-3) and pre-diabetes. A total of sixty clinically ascertained pre-diabetes cases and twenty-five healthy controls were included. Serum IGF-2 and binding proteins were estimated using commercially available ELISA kit. All groups had a positive correlation between all serum parameters. Multinomial logistic regression showed that all the study parameters directly affected each other. The results could not prove any correlation between IGF-2 and its binding proteins during pre-diabetes stage. Further assessments of these factors in larger groups of males and females in diabetic individuals could be useful to support our hypothesis that these factors change only in diabetes mellitus.

The relationship between preptin, Forkhead box protein O1 and mechanistic target of rapamycin levels in prediabetic patients.

Prediabetes is a state of high risk for developing some metabolic disorders. Previous studies have shown that components of some mediators involved in glucose metabolism regulation may have a profound effect during developing prediabetes state. This study investigates the effect of some novel prediabetic-related factors in prediabetes individuals for the first time. Sixty prediabetes (American Diabetes Association criteria) and 25 healthy control subjects were enrolled in the study. Systemic and chronic inflammatory diseases, coronary heart disease, and malignant disease patients were excluded. Anthropometric measurements and fasting glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), lipid profile, preptin, and serum and leuckocyte levels of FOXO-1 and mTOR were determined. The findings showed an elevated level of leukocyte mTOR in the Impaired Glucose Tolerance (IGT) group and leukocyte FOXO-1 in the Impaired Fasting Glucose (IFG) and IGT groups compared to the control group. Moreover, higher levels of serum, and leukocyte FOXO-1 in the control group, and leukocyte mTOR level in the IFG group were detected in females compared to males. There was a positive correlation between all of the studied serum parameters, and a positive correlation between basal glucose concentration and leukocyte mTOR and FOXO-1. According to our results, elevated serum and cellular levels of mTOR in the IGT group and FOXO-1 in IFG and IGT groups may be triggered by increased glucose concentration. Indeed, mTOR-mediated variations in cellular level from female patients and FOXO-1-mediated variations of male patients indicated that these factors might play a critical role in glucose intolerance.

Effects of omega-3 polyunsaturated fatty acid supplementation on serum fetuin-A levels in type 2 diabetic patients.

Fetuin-A is an endogenous inhibitor of the insulin-stimulated insulin receptor tyrosine kinase recently shown that high levels of circulating fetuin-A are associated with insulin resistance in humans suggesting that fetuin-A may represent a novel mechanism involved in the pathophysiology of type 2 diabetes (T2DM). Dietary omega-3 polyunsaturated fatty acids (n-3 PUFAs) are known to reduce triglyceride levels, but their impact on glycemic control are not well known. The aim of this study to determine the effects of omega-3 PUFA supplementation on fetuin-A and glycemic control in patients with type 2 diabetes mellitus. 40 T2DM patients (17 males/23 females; aged 39-65 years) were included in the study. Serum fetuin-A levels and metabolic and biochemical profiles were measured before (baseline) and two months after n-3 PUFA supplementations (1.2 g/day). Serum fetuin-A levels were measured by enzyme-linked immunosorbent assay. Our results indicated that serum fetuin-A, fasting glucose, HbA1c and triglyceride levels were significantly decreased after supplementation (P<0.02, P<0.001, P<0.02 and P<0.01, respectively). At baseline, serum fetuin-A levels were correlated with HbA1c (r:-0.391, P<0.04). A significant positive correlation between fetuin-A and both triglycerides (r: 0.343, P<0.05) and total cholesterol (r: 0.330, P<0.05) and negative correlation between fetuin-A and fasting glucose (r: -0.405, P<0.01) were found after the supplementations. When performed multiply regression analysis, we found that serum fetuin-a levels were related with triglyceride levels (r: 0.351, P<0.01) at baseline and HbA1c levels (r: 0.344, P<0.04) after the supplementation. Based on the results, it thought that omega-3 PUFA intake decreases serum fetuin-A levels and serum fetuin-A is associated with plasma lipids and glycemic controls in type 2 diabetic patients. Further studies are required to resolve the question.

Effects of peritoneal-and hemodialysis on levels of plasma protein and lipid oxidation markers in diabetic patients.

AIM: The aim of this paper was to evaluate the effects of dialysis procedures on oxidative stress in diabetic patients. METHODS: The study was performed on 15 non-diabetic hemodialysis (HD) patients, 30 non-diabetic perinoteal dialysis (PD) patients, 18 diabetic HD patients (DHD), 15 diabetic PD patients (DPD), and 20 healthy controls. Plasma thiobarbituric acid reactive substances (TBARS), protein carbonyl (PCO), and oxidized LDL (oxLDL) were determined as oxidative stress markers. Plasma thiol (P-SH), erythrocyte glutathione (GSH) levels, and serum paraoxonase (PON1) activities were measured as antioxidants. RESULTS: HD patients have significantly higher oxLDL, TBARS and PCO levels and significantly lower P-SH levels than PD patients. DHD patients have significantly higher PCO levels and PON1 activities and significantly lower GSH levels than non-diabetic HD patients. There was no any difference in oxidative stress parameters between DPD and non-diabetic PD patients. CONCLUSION: Oxidative stress is exacerbated by HD in diabetic patients. Treatment strategy with antioxidants in dialysis patients may be associated with a worsened survival.

Role of plasma viscosity and plasma homocysteine level on hyperinsulinemic obese female subjects.

Obesity is associated with atherosclerotic risk factors, including reduced blood flow, endothelial dysfunction, lipid disorders and hyperinsulinemia. In recent years, several studies have demonstrated that elevated homocysteine is a risk factor for atherosclerosis. This study was aimed at determining whether any relationship between plasma viscosity and homocysteine levels in patients with normo and hyperinsulinemic obese patients. Obese women (n=75) and healthy, age-matched non-obese women (n=70) was included in our study. Plasma viscosity, tHcy, insulin level, total-C, LDL-C, HDL-C, triglyceride and glucose level were significantly higher in obese subjects than in non-obese subjects. Obese subjects were also divided into two groups, according to the basal insulin levels as normo and hyper insulinemic. Hyperinsulinemic obese subjects had significantly higher PV level compared with normoinsulinemic subjects. When correlation analyses were performed normoinsulinemic obese subjects, significant correlations were found between PV and total-C (r: 0.776) and insulin level (r: 0.752), BMI (r: 0.580), HOMA-IR (r: 0.510). PV was positively correlated with total-C (r: 0.485), insulin level (r: 0.624), BMI (r: 0.624) and HOMA-IR ratio (r: 0.707), in hyperinsulinemic obese subjects. Hcy was positively correlated BMI in both groups. In conclusion that, it is point out that elevated homocysteine and increased PV are two factors that may act separately and probably do not affect each other.

Attenuation of acute lung injury following lower limb ischemia/reperfusion: the pharmacological approach.

AIM: The purpose of this study was to examine the effects of N-acetylcysteine (NAC), calcium dobesilate (DOBE) and aprotinin on the amelioration of lung damage following ischemia/reperfusion injury in a rat hind limb model. A well known antioxidant dimethyl-sulfoxide (DMSO) was also tested for comparison. METHODS: Ischemia was induced in the lower limb for 4 h by vascular clamping and followed by 1 h of reperfusion. Lung injury was evaluated in 5 groups as a saline (control), DMSO, NAC, DOBE and aprotinin group. Plasma creatine kinase, lactate dehydrogenase, thiobarbituric acid reactive substances (TBARS) as well as lung tissue TBARS levels were measured. Lung tissue samples were taken for histological examination. P<0.005 was considered statistically significant. RESULTS: Plasma TBARS values were found to be significantly lower in the DMSO (P<0.005), NAC (P<0.005) and aprotinin (P<0.005) groups compared to the control group. Lung TBARS values were significantly lower in the DMSO, NAC, DOBE and aprotinin groups compared to the control group (P<0.001, P<0.001, P<0.001). Also in the aprotinin group lung TBARS values were found to be significantly lower compared to DMSO (P<0.001), NAC (P<0.001) and DOBE (P<0.001) groups. Histological examination showed less prominent peribronchial leukostasis (P<0.005) and interstitial leukostasis (P<0.005) in all drug groups compared to the control group. CONCLUSION: These observations indicate that DOBE and NAC, which are known to have antioxidant properties and aprotinin, a serine proteinase inhibitor, acted effectively on the prevention of lung injury in a rat hind limb ischemia/reperfusion model. The reason why aprotinin exerts a more protective effect than the other drugs is not clear, however, its clinical use may have the dual advantage of hemostasis and lung protection in surgical practice.

The relationship between antioxidant enzymes and bladder cancer.

Carcinogenesis proceeds through at least three distinct stages - initiation, promotion and progression. Free radicals play an important role in the multistep complex course of carcinogenesis. Urinary bladder has been recognized as a target organ for many carcinogens, including benzidine, beta-napthylamine, 2 napthylamine, 4-aminobiphenyl. Antioxidants have been shown to inhibit both initiation and promotion in carcinogenesis. The aim of presented study was to determine and compare the oxidant and antioxidant status in different clinical stages of bladder cancer and of control groups. Study was conducted in fifty-two (n=52) patients with transitional cell epithelial cancer of bladder and in twenty-four (n=24) healthy adults as plasma and erythrocyte controls. Malondialdehyde levels (4.636+/-1.118, 2.853+/-0.576 / 262.112+/-61.772, 203.788+/-35.340) were significantly higher and erythrocyte glutathione levels (6.272+/-1.708, 7.523+/-1.346) were significantly lower in bladder cancer patients group than in control group. Erythrocyte glutathione reductase and glutathione peroxidase (3.935+/-1.155, 5.481+/-1.626 / 8.729+/-1.614, 12.362+/-1.707) activities were significantly lower in cancer patients. In the other hand, glutathione S-transferase activities (3.100+/-1.177, 1.071+/-0.471) were found significantly increases. We suggest that the values of glutathione S-transferase enzyme activity can be used for a tumor detection approach and even as an indicator of the biological behavior of the bladder carcinoma.

Urinary excretion of sialic acid in patients with bladder tumors.

The pre- and post-treatment urinary total sialic acid/creatinine (TSA/Cr) ratios of patients with bladder tumor (n = 60) were determined. We found a significant increase in the mean urinary TSA/Cr ratio in patients with bladder tumors than in healthy people (99.80 +/- 15.60 micrograms/g Cr, 52.57 +/- 15.60 micrograms/g Cr, P < 0.001). We determined that the mean post-treatment TSA/Cr ratio of 44 patients was significantly lower than their pretreatment ratio and this value also decreased to the level in healthy people. (TSA/Cr; healthy people, 52.57 +/- 15.60 micrograms/g Cr, P < 0.001). The patients with decreased TSA/Cr ratio in the post-treatment period showed complete or partial regression of their disease. In 8 patients, urinary TSA/Cr ratio in the post-treatment period increased to 105 +/- 14.5 micrograms/g Cr value. In clinical and pathologic evaluation, it was shown that disease progressed in all of these 8 patients. The mean post-treatment TAS/Cr ratio of 8 patients did not differ from the pretreatment ratio (87.44 +/- 20.20 micrograms/Cr) and it was shown that their clinical status did not change. These findings show that urinary excretion of TSA correlates with the clinical status of bladder tumor and it could be used to follow the course of the disease, and follow-up treatment.

Urinary excretion of sialic acid in patients with superficial bladder tumors.

Urinary total sialic acid/creatinine (TSA/Cr) ratio was determined in 73 patients with superficial bladder tumors and 34 healthy volunteers. The mean TSA/Cr value in the tumor group was higher than the control group (P < 0.001) and this difference was significant. Comparing the urinary TSA/Cr ratio of Tl, Ta, grade I-II, grade III, single, multiple, primary and recurrent tumors, with the control group revealed significant results (P < 0.001). Therefore the urinary TSA/Cr ratio determination in the follow-up of these patients may be used as a non-invasive procedure.

The susceptibility of red blood cells to autoxidation in type 2 diabetic patients with angiopathy.

We examined the in vitro susceptibility of red blood cell (RBC) lipids to oxidation in type 2 diabetic patients with or without angiopathy. Lipid peroxidation was assessed by quantifying thiobarbituric acid (TBA) reactivity as malondialdehyde (MDA). We also examined the RBC antioxidant status by determining glutathione (GSH) levels. Before in vitro oxidation, RBC MDA levels were significantly higher in both diabetic groups than in the controls (P < .001), and a significant difference was found between the two diabetic groups (P < .05). After in vitro treatment of RBCs with hydrogen peroxide, the degree of lipid peroxidative damage was significantly higher in diabetic patients with angiopathy versus diabetics without angiopathy (P < .001). Diabetic patients have low RBC GSH levels compared with controls, and after in vitro oxidation, the levels were significantly decreased in diabetics (P < .001). There was not a significant correlation between RBC MDA levels and glycated hemoglobin (GHb), plasma cholesterol, and triglyceride. The correlation between RBC MDA and GSH was weak (P < .001). We suggest that the results of this study might help to clarify the role of oxidative mechanisms as an in vitro model of degenerative damage in type 2 diabetic angiopathic complications.

Susceptibility of erythrocyte lipids to oxidation and erythrocyte antioxidant status in myocardial infarction.

OBJECTIVE: We evaluated the erythrocyte lipid susceptibility to oxidation and erythrocyte antioxidant status in patients with myocardial infarction (MI). DESIGN AND METHODS: Patients with MI were divided into two group according to the severity of the disease as severe (n = 30) or milder (n = 25). Malondialdehyde as a marker of lipid peroxidation was measured to show the lipid susceptibility to oxidation. Erythrocytes were stressed in vitro by hydrogen peroxide acting as the oxidative agents for 120 min. After designated time, erythrocyte MDA production was significantly higher in patients with severe MI than in controls and in patients with milder MI (p < 0.001, p < 0.001, respectively). Antioxidant status was determined by measuring the reduced glutathione levels and glutathione peroxidase activity of erythrocyte. RESULTS: In patients with MI, antioxidant status was significantly lower than in controls, and there was no significant difference between the patient groups. CONCLUSION: Determination of erythrocyte lipid susceptibility to oxidation may be a useful in vitro test to evaluate the degree of oxidative stress in myocardial infarction.

Effects of cyclosporin A and ibuprofen on liver ischemia-reperfusion injury in the rat.

Liver ischemia followed by reperfusion is an important and common clinical event associated with the activation of an endogenous inflammatory response. The aim of this study was to determine the effects of cyclosporin A (CsA) and ibuprofen (IBU) on ischemia-reperfusion injury. Male Spraque-Dawley rats were subjected to 60 min of total liver ischemia followed by 120 min reperfusion. Liver tissue samples were obtained for measurements of malondialdehyde (MDA) levels as an index of tissue lipid peroxidation by thiobarbituric acid assay. Three groups of animals were pre-treated with CsA or IBU or both. Treatment with these agents was given at onset reperfusion after ischemia. The other groups were designated as ischemic controls, non-ischemic controls and reperfusion group without treatment. Ischemic control animals showed increased liver MDA levels and in the reperfusion group MDA levels were significantly higher than ischemic levels. CsA and IBU-treated animals had better survival and diminished liver MDA levels. The most significant decrease MDA levels was observed in the group treated with two agents which were given together. Serum enzyme levels were significantly higher in the reperfusion group than in the ischemic controls and the enzyme levels were significantly diminished after the treatments. This study suggests that CsA and IBU may be important agents in modulating lipid peroxidation in ischemia-reperfusion liver injury, and combined therapy with these agents may be more effective in treatment of ischemia-reperfusion injury.

A study on the carotid artery intima-media thickness and its association with lipid peroxidation.

High resolution B-mode ultrasonography of the carotid arteries has been used to investigate the signs of early atherosclerotic vessel wall disease by measuring the intima-media thickness (IMT). We examined the association between IMT and lipid peroxidation and found IMT to be increased in a group of patients with respect to controls (1.430+/-0.341 mm versus 0.703+/-0.201 mm, P < 0.001). Plasma and erythrocyte malondialdehyde (MDA) levels were also significantly higher (P<0.001) and the erythrocyte reduced glutathione (GSH) levels were significantly lower (P <0.001) in the patients with respect to the controls. In the groups of patients there was no significant correlation between the mean IMT and the plasma and erythrocyte MDA levels or the erythrocyte GSH levels. In conclusion determination of lipid peroxides would be especially important and advisable in patients with increased carotid IMT. Type II diabetes and hypertension were also associated with increased IMT.

Plasma leptin levels in obese and non-obese postmenopausal women before and after hormone replacement therapy.

OBJECTIVE: the aim of this study was to investigate the effect of hormone replacement therapy (HRT) on plasma leptin levels in postmenopausal women, and the relationship between the plasma leptin levels and obesity. METHODS: premenopausal women with normal cycles (n=30; mean ages, 35.4+/-8.3 years) and postmenopausal women (n=45; mean ages, 49.5+/-4.7 years) were randomly selected. Women were classified as obese (BMI>27 kg/m(2)) and as non-obese (BMI<27 kg/m(2)). Blood samples were obtained from the premenopausal women at the beginning of cycle, and from the postmenopausal women before and 6 months after HRT. Plasma leptin levels were measured by radioimmunassay. RESULTS: plasma leptin levels were significantly higher in premenopausal women than in postmenopausal women (18. 60+/-5.0; 3.67+/-2.44 ng/ml, respectively, P<0.001). Obese premenopausal women (n=15) had significantly higher plasma leptin levels (24. 60+/-7.81 ng/ml) in comparison with the levels of the non-obese premenopausal women (n=15; 12.50+/-4. 63 ng/ml) (P<0.001). Although there was no significant difference in the plasma leptin levels between obese (n=25) and non-obese (n=20) postmenopausal women before HRT, plasma leptin levels were significantly elevated in both obese and non-obese postmenopausal women after HRT (P<0.001), and the obese women had significantly higher plasma leptin levels than the non-obese (29.05+/-10.53; 14.78+/-6.76 ng/ml, respectively, P<0.001). CONCLUSION: HRT is effective in the elevation of the plasma leptin levels in postmenopausal women, and in obese women the increase of the plasma leptin levels are more marked than the non-obese women after HRT.

Effects of hormone replacement therapy on plasma nitric oxide and total thiol levels in postmenopausal women.

Improvement in endothelial function may be an important mechanism by which hormone replacement therapy (HRT) protects postmenopausal women against coronary artery disease. Our aim was to assess the effects of HRT on plasma nitric oxide (NOx) (nitrate plus nitrite) and total thiols in postmenopausal women, as these parameters are associated with enhanced endothelial functions. Thirty-five healthy postmenopausal volunteers (mean age 50.5 +/- 4.7 yr) in an academic and hospital research environment were involved in the study. Blood samples were collected, one at baseline and the second after 6 mo of HRT. Plasma NOx and total thiol levels were significantly elevated in the subjects after HRT. NOx may be of importance in the protective effects of HRT. Further, the increase of plasma antioxidant thiol levels might also contribute to the beneficial effects of HRT.

Effects of oxidative stress on the erythrocyte Na+,K+ ATPase activity in female hyperthyroid patients.

This study was planned to determine the effects of free-radical-induced damage on the Na+,K+-ATPase activity of erythrocytes during hyperthyroidism and 4 wk after propylthiouracil (PTU) therapy (400 mg/d). The levels of plasma thiobarbituric acid-reactive substances (TBARS) as a marker of lipid peroxidation, erythrocyte glutathione (GSH) concentration as an antioxidant, blood ATP concentration, and erythrocyte membrane Na+,K+-ATPase activity were determined in female hyperthyroid patients (n = 22, mean age 40.5 +/- 6.5 yr). Before the PTU therapy, plasma TBARS concentration was significantly higher and the levels of blood ATP and erythrocyte GSH and the activity of membrane Na+,K-+-ATPase were significantly lower in the hyperthyroid patients (n = 15 women, mean age 40.8 +/- 7.3 yr). Four weeks after PTU therapy, plasma TBARS concentration was decreased, and levels of erythrocyte GSH and blood ATP and of Na+,K+-ATPase activity of erythrocytes were elevated in the treated patients. There was a significant positive correlation between blood ATP concentration and Na+,K+-ATPase activity, and a negative correlation between plasma TBARS concentration and Na+,K+-ATPase activity before PTU. Our results might help to clarify the effects of the oxidative mechanisms on the erythrocyte membrane Na+,K+-ATPase activity in hyperthyroid patients.

Trace element levels in the experimental peritonitis.

Electron transfer from iron or copper ions to oxygen is an important example of cellular free radical initiation. Oxygen derived free radicals have been implicated as mediators of cellular injury in several model systems. To evaluate the importance of iron, copper and zinc levels on lipid peroxidation in peritonitis, we measured peritoneum malondialdehyde (MDA) as a marker of lipid peroxidation, zinc, copper, and iron levels during an animal model of intraperitoneal sepsis. Additionally the effects of the free radical scavenger alpha-tocopherol administration was studied. The peritoneum MDA, iron, copper and zinc levels were increased after induction of peritonitis with Escherichia Coli. The treatment with alpha-tocopherol was decreased the peritoneum MDA, iron and copper levels significantly, except the zinc level (p < 0.001, p < 0.001, p < 0.001, respectively). Additionally the alpha-tocopherol treatment for three days prior to injection of E.Coli more decreased MDA, copper and iron levels than that of the treatment with alpha-tocopherol at the time of injection of E. Coli (p < 0.001, p < 0.001, p<0.001, respectively). Our results indicated that copper, iron and zinc had important effects on peroxidation events in E. Coli induced peritonitis, and alpha-tocopherol treatment can improve the oxidant status.