Leptin and adiponectin levels in obstructive sleep apnea phenotypes.

Objective: To examine the serum levels of leptin and adiponectin in different obstructive sleep apnea (OSA) phenotypes. Methods: Obese patients who were admitted to our sleep laboratory were included. All patients underwent spirometry, daytime arterial blood gas analysis, polysomnography and transthoracic echocardiography. Serum levels of adiponectin and leptin were recorded. Results: Analysis included 146 OSA patients (81 females, 65 males, age: 49.8 ± 10.7 years, body mass index: 40.3 ± 4.9 kg/m2, 47.9% severe OSA, 42.5% severe obesity). Females had higher leptin and adiponectin levels (p < 0.001; p < 0.001, respectively). Leptin levels were higher in patients with severe obesity (p < 0.001). Severe OSA patients had lower leptin and adiponectin levels (p = 0.023; p = 0.035, respectively). Conclusion: Adipokine levels were different especially in OSA patients with severe obesity, female gender and severe OSA.

A Comparison of hs-CRP Levels in New Diabetes Groups Diagnosed Based on FPG, 2-hPG, or HbA1c Criteria.

Fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c) have been used to diagnose new-onset diabetes mellitus (DM) in order to simplify the diagnostic tests compared with the 2-hour oral glucose tolerance test (OGTT; 2-hPG). We aimed to identify optimal cut-off points of high sensitive C-reactive protein (hs-CRP) in new-onset DM people based on FPG, 2-hPG, or HbA1c methods. Data derived from recent population-based survey in Turkey (TURDEP-II). The study included 26,499 adult people (63% women, response rate 85%). The mean serum concentration of hs-CRP in women was higher than in men (p < 0.001). The people with new-onset DM based on HbA1c had higher mean hs-CRP level than FPG based and 2-hPG based DM cases. In HbA1c, 2-hPG, and FPG based new-onset DM people, cut-off levels of hs-CRP in women were 2.9, 2.1, and 2.5 mg/L [27.5, 19.7, and 23.5 nmol/L] and corresponding values in men were 2.0, 1.8, and 1.8 mg/L (19.0, 16.9, and 16.9 nmol/L), respectively (sensitivity 60-65% and specificity 54-64%). Our results revealed that hs-CRP may not further strengthen the diagnosis of new-onset DM. Nevertheless, the highest hs-CRP level observed in new-onset DM people diagnosed with HbA1c criterion supports the general assumption that this method might recognize people in more advanced diabetic stage compared with other diagnostic methods.

Effects of spironolactone on residual renal function and peritoneal function in peritoneal dialysis patients.

There is increasing evidence that long-term peritoneal dialysis (PD) is associated with structural changes in the peritoneal membrane. Inhibition of the renin-angiotensin system has been demonstrated to lessen peritoneal injury and to slow the decline in residual renal function. Whether spironolactone affects residual renal function in addition to the peritoneal membrane is unknown. We evaluated 23 patients (13 women) with a glomerular filtration rate of 2 mL/min/1.73 m2 or more who were receiving PD. Patients with an active infection or peritonitis episode were excluded. Baseline measurements were obtained for serum high-sensitivity C-reactive protein (hs-CRP), vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta), and connective tissue growth factor (CTGF); for daily ultrafiltration (in milliliters); for end-to-initial dialysate concentration of glucose (4/D0 glucose), Kt/V, and peritoneal transport status; and for dialysate cancer antigen 125 (CA125). Spironolactone therapy (25 mg) was given daily for 6 months, after which all measurements were repeated. Mean age of the patients was 46 +/- 13 years. Duration of PD was 15 +/- 21 months (range: 2-88 months). After spironolactone therapy, mean dialysate CA125 was significantly increased compared with baseline (20.52 +/- 12.06 U/mL vs. 24.44 +/- 13.97 U/mL, p = 0.028). Serum hs-CRP, VEGF, TGF-beta, CTGF, daily ultrafiltration, D/Do glucose, Kt/V and peritoneal transport status were similar at both times. At the end of the study period, residual glomerular filtration rate in the patients was lower. In PD patients, treatment with spironolactone seems to slow the decline of peritoneal function, suppress the elevation of profibrotic markers, and increase mesothelial cell mass.

Elevated resistin levels are associated with inflammation in hemodialysis patients with failed renal allografts.

BACKGROUND: Resistin is an adipocytokine, associated with insulin resistance and inflammation. The aim of this study is to evaluate the levels of serum resistin levels and other markers of inflammation in hemodialysis (HD) patients with failed renal allografts. METHODS: Sixty-nine HD patients with failed renal allografts and 98 never transplanted (naive) HD patients and also 21 healthy controls were included in the study. Serum levels of various biochemical parameters as well as resistin, IL-6, TNF-α and hs-CRP as biochemical markers of inflammation, were measured. RESULTS: Serum resistin levels in patients with failed renal allografts (4.80 ± 2.06 ng/mL) were significantly higher than those of the naive HD patients (3.44 ± 1.48 ng/mL) and healthy controls (0.95 ± 0.38 ng/mL; p<0.001). Patients with failed transplants were also characterized by higher TNF-alpha levels (96.8 ± 131.3 pg/mL vs. 40.9 ± 25.4 pg/mL; p<0.001) and IL-6 levels (83.9 ± 150.9 pg/mL vs. 14.6 ± 14.4 pg/mL; p<0.001) as compared to naive HD patients. Serum hs-CRP levels in patients with failed renal allografts (9.33 ± 11.86 mg/L) were significantly higher than those of the naive HD patients (1.26 ± 1.71 mg/L) and healthy controls (2.12 ± 1.82 mg/L; p<0.001). Serum albumin levels in patients with failed transplants (3.84 ± 0.47 g/dL) were lower as compared to never transplanted HD patients (4.13 ± 0.33 g/dL) and healthy controls (4.53 ± 0.40 g/dL; p<0.001). There was a positive correlation between serum resistin and TNF-alpha levels (r = 0.486, p<0.001). CONCLUSIONS: Serum resistin levels are increased in HD patients with failed renal allografts very probably reflecting an allograft-induced chronic inflammatory state.

Twelve-year trends in the prevalence and risk factors of diabetes and prediabetes in Turkish adults.

There is concern about an emerging diabetes epidemic in Turkey. We aimed to determine the prevalence of diagnosed and undiagnosed diabetes, prediabetes and their 12-year trends and to identify risk factors for diabetes in the adult Turkish population. A cross-sectional, population-based survey, 'TURDEP-II' included 26,499 randomly sampled adults aged ≥ 20 years (response rate: 87 %). Fasting glucose and biochemical parameters were measured in all; then a OGTT was performed to identify diabetes and prediabetes in eligible participants. The prevalence of diabetes was 16.5 % (new 7.5 %), translating to 6.5 million adults with diabetes in Turkey. It was higher in women than men (p = 0.008). The age-standardized prevalence to the TURDEP-I population (performed in 1997-98) was 13.7 % (if same diagnostic definition was applied diabetes prevalence is calculated 11.4 %). The prevalence of isolated-IFG and impaired glucose tolerance (IGT), and combined prediabetes was 14.7, 7.9, and 8.2 %, respectively; and that of obesity 36 % and hypertension 31.4 %. Compared to TURDEP-I; the rate of increase for diabetes: 90 %, IGT: 106 %, obesity: 40 % and central obesity: 35 %, but hypertension decreased by 11 % during the last 12 years. In women age, waist, body mass index (BMI), hypertension, low education, and living environment; in men age, BMI, and hypertension were independently associated with an increased prevalence of diabetes. In women current smoking, and in men being single were associated with a reduced risk. These results from one of the largest nationally representative surveys carried out so far show that diabetes has rapidly become a major public health challenge in Turkey. The figures are alarming and underscore the urgent need for national programs to prevent diabetes, to manage the illness and thus prevent complications.

Decrease in endothelial progenitor cells associated with inflammation, but not with endothelial dysfunction in chronic hemodialysis patients.

INTRODUCTION: Endothelial progenitor cells (EPC), bone marrow derived cells, are considered to have a pivotal role in maintaining the integrity and repair of the endothelium. Endothelial dysfunction, atherosclerosis and inflammation are implicated for increased CV mortality in uremia. In this study, we aimed to investigate the possible association of EPC with inflammation, endothelial dysfunction and atherosclerosis in chronic hemodialysis (HD) patients. PATIENTS AND METHODS: 67 HD patients (male/female: 30/37, mean age: 58 ± 15 years) and 22 healthy controls (male/female: 13/9; mean age: 48 ± 8 years) were included. EPC were cultivated in the fibronectin-covered culture dishes and counted. Also EPC markers were studied by flow cytometry using anti-CD34, anti-CD133 and anti-vascular endothelial growth factor receptor 2 (VEGFR-2) antibodies. Serum levels of IL-6, TNF-α, intercellular cell adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) and asymmetric dimethyl-arginine (ADMA) were measured by ELISA method. Endothelial function was investigated by measuring flow-mediated dilatation (FMD) of the brachial artery. Carotid intima-media thickness (CIMT) and ratio (CIMR) were also examined. RESULTS: EPC number was decreased in HD patients when compared to controls (63.7 ± 8.9 vs. 101.5 ± 19.6/ high power field, p < 0.001). Also CD34+ cell count was significantly lower in the HD group (2.26 ± 3.52 vs. 6.03 ± 4.73%, p < 0.0001). EPC number was significantly inversely correlated with serum TNF-α levels in HD patients(r: -0.453, p < 0.001) and also in the control group (r = -0.509, p = 0.044). There was an inverse association between VEGFR-2+/CD34+cell count and serum IL-6 levels (r: -0.364, p = 0.006) in HD patients. However, EPC count was not related to FMD and CIMT/CIMR. In HD patients, there was a positive correlation between serum IL-6 levels with CIMT (r = 0.358, p = 0.01) and CIMR was positively correlated with serum ICAM (r = 0.430, p = 0.002). CONCLUSION: EPC number was decreased in uremia and was associated with inflammation. TNF-α might have specific inhibitory actions on EPC in both HD patients and healthy controls. No relationship was present between EPC and endothelial dysfunction/atherosclerosis.

Adiponectin, leptin and ghrelin levels in obese adolescent girls with polycystic ovary syndrome.

STUDY OBJECTIVE: To evaluate the differences in adipokines, namely adiponectin, leptin, and ghrelin, in obese adolescent girls with or without polycystic ovary syndrome (PCOS). DESIGN: Case-control study. SETTING: University hospital. PARTICIPANTS: 38 adolescent girls (age 15-20 years). Group I: 17 Obese adolescent girls with PCOS (BMI ≥ 30 kg/m(2)); Group II: Control group of 21 obese adolescent girls (BMI ≥ 30 kg/m(2)). MAIN OUTCOME MEASURES: Adiponectin, leptin, and ghrelin measurements. RESULTS: LH, LH/FSH, and cortisol levels were significantly higher in the obese PCOS girls compared to the obese controls (6.94 ± 3.28 vs 4.44 ± 1.79; 1.50 ± 0.72 vs 0.90 ± 0.36; 16.02 ± 4.28 vs 12.46 ± 5.29; P < .05, respectively). Adiponectin, leptin, and ghrelin levels were similar between the obese PCOS girls and the obese controls (11.13 ± 6.00 vs 15.26 ± 12.66; 23.66 ± 11.54 vs 23.11 ± 11.17; 665.69 ± 402.12 vs 650.22 ± 467.73, respectively). Adiponectin negatively correlated with BMI (r = -0.32; P = .04) and positively correlated with fasting glucose (r = 0.40; P = .01). Leptin positively correlated with BMI (r = 0.534; P = .001), estradiol (r = 0.354; P = .02), and TSH (r = 0.374; P = .02). No significant correlation was found between ghrelin and the test parameters. CONCLUSION: Among obese adolescents with PCOS, adiponectin, and leptin levels do not seem to be determined by the existence of PCOS, while ghrelin presents no significant correlation.

Lower serum prohepcidin levels associated with lower iron and erythropoietin requirements in hemodialysis patients with chronic hepatitis C.

BACKGROUND: Patients with chronic HCV infection have increased liver iron. Recently identified protein hepcidin synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Lower erythropoietin and iron supplementation requirements were previously reported in HD patients with HCV infection. We investigated the association of prohepcidin with inflammation and iron parameters in HD patients with and without chronic HCV infection. METHODS: Sixty patients (27 male, 33 female, mean age 50±15 years) on chronic HD were included. Parameters related to iron metabolism (ferritin, serum iron and total iron binding capacity (TIBC)), inflammation (hs-CRP, TNF-α and IL-6) and prohepcidin levels were measured. The response to treatment (erythropoiesis-stimulating agent (ESA) resistance index) was assessed from the ratio of the weekly erythropoietin (rhuEPO) dose to hemoglobin (Hb) per unit weight. RESULTS: Serum prohepcidin levels of HCV positive patients (135±25 ng/mL) were significantly lower than HCV negative patients [148±18 ng/mL, (p=0.025)]. Serum IL-6 levels of HCV positive patients were also significantly lower than HCV negative patients (p=0.016). Serum prohepcidin levels were positively correlated with ferritin (r=0.405, p=0.001) and IL-6 (r=0.271, p=0.050) levels in HD patients. In the HCV positive group, serum prohepcidin levels significantly correlated with ferritin levels (r=0.514 p=0.004). In the HCV negative group, serum prohepcidin levels significantly correlated with serum IL-6 levels (r=0.418, p=0.027). In multiple regression analysis performed to predict prohepcidin in HCV positive patients, serum ferritin was found to be an independent variable (r=0.28, p=0.008). CONCLUSIONS: HCV positive HD patients have low levels of serum prohepcidin and IL-6 which might account for iron accumulation together with lower iron and rhuEPO requirements in these patients.

Prevalence of pituitary adenomas in macroprolactinemic patients may be higher than it is presumed.

One form of prolactin (PRL) is macroprolactin with high molecular mass. Many macroprolactinemic patients have no pituitary adenomas and no clinical symptoms of hyperprolactinemia, it is controversial whether macroprolactinemia is a benign condition that does not need further investigation and treatment. In this study, we aimed to compare macroprolactinemic patients (group I) with the true hyperprolactinemic patients (group II) for the presence of pituitary adenoma. We investigated 161 patients with hyperprolactinemia, whose magnetic resonance imaging records of the pituitary were taken. All patients were questioned for irregular menses, infertility and examined for galactorrhea. Patients were screened for macroprolactinemia by polyethylene glycol precipitation, and a recovery of ≤40% and normal monomeric PRL level was taken as an indication of significant macroprolactinemia. Of 161 patients with hyperprolactinemia, 60 (37.26%) had macroprolactinemia. PRL levels of group II were lower than those of group I (P = 0.011), although monomeric PRL levels of group II were higher than those of group I (P = 0.0005). Of 60 macroprolactinemic patients, 16 (26.7%) had pituitary adenomas. The prevalence of pituitary adenomas was lower in group I, compared with group II (P = 0.0005). No significant differences were found between the prevalences of irregular menses and infertility of group I and II (P = 0.084, P = 0.361). Prevalence of galactorrhea in group I was lower than that in group II (P = 0.048). Prevalence of pituitary adenomas in macroprolactinemic patients is lower compared with the true hyperprolactinemic patients, but may be higher than that found in other recent studies and in the general population.

Serum adipokines and low density lipoprotein subfraction profile in hypopituitary patients with growth hormone deficiency.

The aim was to evaluate the concentrations of lipid subfractions in relation to adipokines and metabolic parameters in adult growth hormone (GH)-deficient hypopituitary patients on conventional replacement therapy. The study included 21 GH deficient-hypopituitary patients (age: 36.0 ± 15.1 years, male/female: 7/14) on conventional replacement therapy other than GH and 20 comparable controls (age: 37.3 ± 14.0 years, male/female: 6/14). Lipid subfractions (Lipoprint system), serum adipokine (leptin, adiponectin, resistin) concentrations, body composition, a surrogate marker for insulin resistance (HOMA) and conventional lipid profile were evaluated. No statistically significant difference was found with respect to HOMA, adipokine concentrations and anthropometric parameters between patients and controls except for significantly increased waist-to-hip ratio in hypopituitary group. Total and LDL cholesterol concentrations were significantly higher in the patients. LDL particle size (268.88 ± 3.16 vs. 271.31 ± 3.11 Å, P = 0.151) and small-dense LDL subfraction did not differ significantly. According to logistic regression analysis, triglyceride concentrations ≥1.69 mmol/L was the sole parameter significantly and independently predicted small (<268 Å) LDL particle size (P = 0.019) in the whole group. Increased triglyceride concentrations affect LDL particle size in GH-deficient hypopituitary patients. Small dense LDL seems not directly contribute to atherogenic potential in hypopituitarism.

Comparison of markers of appetite and inflammation between hemodialysis patients with and without failed renal transplants.

OBJECTIVE: The survival of patients returning to hemodialysis (HD) following kidney transplant failure is unfavorable. However, the factors responsible for this poor outcome are largely unknown; chronic inflammation due to failed allograft and malnutrition may contribute to morbidity and mortality. We aim to compare the markers of appetite and malnutrition, and their relation with inflammation in HD patients with and without previous kidney transplantation. METHODS: Fifty-six patients with failed renal allografts at least 3 months on dialysis (31 men, 25 women; mean age, 46 ± 9 years) and 77 HD patients who never underwent a transplant (43 men, 34 women; mean age, 50 ± 15 years) were included in the study. The appetite and diet assessment tool (ADAT) was used to determine the self reported appetite of patients. Serum concentrations of ghrelin, leptin, insulin like growth factor 1 (IGF-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and high-sensitivity C-reactive protein (hs-CRP) were measured. Associations among these variables were analyzed. RESULTS: There were no significant differences considering age, gender or duration of renal replacement therapy between the 2 groups. The scores from Appetite and Diet Assessment Tool were significantly higher in the failed-transplant group. Serum ghrelin levels were significantly higher and serum albumin levels were significantly lower in the failed-transplant group. Serum leptin levels were similar between 2 groups. In addition, hs-CRP, IL-6, and TNF-α levels, which were used as inflammatory parameters, were significantly higher in the failed-transplant group. CONCLUSIONS: Elevated serum ghrelin levels and inflammation may cause diminished appetite and malnutrition in patients with failed renal allografts, and higher levels of this hormone seem to be associated with inflammation caused by retained failed allografts.

Effects of vitamin D replacement therapy on serum FGF23 concentrations in vitamin D-deficient women in short term.

OBJECTIVE: Fibroblast growth factor 23 (FGF23), a phosphatonin, inhibits renal phosphate reabsorption and suppresses 1-α hydroxylase activity. Calcitriol stimulates FGF23 synthesis in bone. We aimed to determine the effect of vitamin D replacement therapy on serum FGF23 concentrations in vitamin D-deficient women and to compare the FGF23 concentrations of vitamin D-deficient patients with healthy subjects and patients with genetically determined hypophosphatemic rachitis. DESIGN AND METHODS: The study group was composed of vitamin D-deficient females (n=18, mean age 29.1 ± 9.9 years), vitamin D-sufficient healthy females (control group; n=19, mean age 28.5 ± 5.2 years), and patients with genetically determined hypophosphatemic rachitis (n=13, mean age 26.5 ± 15.1 years). The groups were compared for serum FGF23, 1,25-dihydroxyvitamin D3 (1,25(OH)2D), calcium, phosphate, bone turnover markers, intact parathyroid hormone (PTH), and urinary excretion of calcium and phosphate. The vitamin D-deficient group was re-evaluated after a standard treatment regimen. RESULTS: Serum FGF23 concentrations were significantly lower in vitamin D-deficient patients than in vitamin D-sufficient women and hypophosphatemic rachitis group. Serum FGF23 and phosphate concentrations further decreased significantly during replacement of vitamin D (P<0.05). A significant negative correlation was evident between FGF23 and PTH before vitamin D replacement in the patients (r=-0.469, P<0.05). CONCLUSION: Decreased FGF23 concentrations, which further decline during vitamin D replacement therapy, may have favorable action on bone mineralization by counterregulatory effect on phosphate homeostasis. Lower 1,25(OH)2D concentrations at baseline and hypophosphatemia during treatment may have dominating effects on FGF23 concentrations in vitamin D deficiency, leading to decreased FGF23 concentrations at baseline and during replacement therapy.

Decrease in mitochondrial oxidative protein damage parameters in the streptozotocin-diabetic rat.

BACKGROUND: Many authors have shown that hyperglycemia leads to an increase in oxidative protein damage in diabetes. The aim of this study was to reveal the susceptibility of mitochondria from liver, pancreas, kidney, and skeletal muscle of diabetic Sprague-Dawley rats, a model of type 1 diabetes, to oxidative protein damage. METHODS: Mitochondrial fractions were obtained by differential centrifugation. To show the effect of hyperglycemia in promoting oxidative protein damage, we determined mitochondrial protein carbonyl, total thiol, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels. The levels of the studied markers, except nitrotyrosine, were determined by colorimetric methods. Nitrotyrosine levels were measured by ELISA. All values were compared with those of the controls by using the Mann-Whitney U-test. RESULTS: Nitrotyrosine and lipid hydroperoxide levels were decreased and other parameters were not changed in liver mitochondria of diabetic rats. Protein carbonyl, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels were decreased and total thiol levels were not changed in pancreas mitochondria of diabetic rats. Only advanced oxidation protein products and lipid hydroperoxide levels were decreased in kidney mitochondria of diabetic rats. The levels of the same parameters were not significantly different in muscle mitochondria of diabetic rats. CONCLUSIONS: The decrease in mitochondrial oxidative protein damage in diabetes may correspond to either an increase in antioxidant defense mechanisms or a different adaptive response of the cells to the increased extramitochondrial oxidative stress in diabetes. The mitochondrial oxidative protein damage-lowering mechanisms in diabetes remain to be clarified.

Relation of aging with oxidative protein damage parameters in the rat skeletal muscle.

OBJECTIVES: An increase in oxidative stress may contribute to the development of oxidative protein damage in the aging rat skeletal muscle. Our aim was to reveal protein carbonyl (PCO), advanced oxidation protein products (AOPP), a novel marker of oxidative stress, and protein thiol (P-SH) levels as markers of protein oxidation, as well as lipid hydroperoxide (LHP) levels as a marker of lipid peroxidation, and relation of nitrotyrosine (NT) levels with these markers in skeletal muscle tissue of young, adult, and old male Wistar rats. DESIGN AND METHODS: In the present study, we investigated the relation between aging and oxidative protein damage parameters such as PCO, NT, AOPP, and P-SH, as well as oxidative stress parameters such as total thiol, nonprotein thiol, and LHP in the skeletal muscle tissue of young, adult, and old Wistar rats. RESULTS: PCO and NT levels of old rats were significantly increased compared with those of young and adult rats. Skeletal muscle AOPP levels were significantly increased in old rats compared with those of adult rats. P-SH levels were significantly decreased in old rats compared with those of young rats. CONCLUSIONS: The finding that the increase in PCO levels of young vs. old group was more significant than that of adult vs. old group may suggest that PCO formation is an early specific marker of aging process in skeletal muscle. In addition, increased levels of nitrotyrosine in the skeletal muscle of the old rat group may be a novel specific marker of oxidative protein damage in the aging muscle. The absence of correlation between oxidative protein damage markers mentioned above and LHP levels may indicate that protein oxidation and lipid peroxidation in the aging rat skeletal tissue are two distinct mechanisms.

Relation between bladder cancer and protein oxidation.

DNA, protein oxidation and lipid peroxidation possess a major impact in carcinogenesis. Also, inflammatory and oxidative events have remarkable importance in bladder cancer. Thus, in this study total protein, protein carbonyl, nitrotyrosine, thiol residues, non-protein thiols, lipid peroxidation, and also, because of their relations to the above parameters, iron and iron binding levels have been investigated in patients with bladder cancer and in control group. Statistical evaluation of the results demonstrated significantly lower plasma protein levels in the patients with bladder cancer, as compared to the healthy control group. Serum iron levels in patients with invasive bladder cancer were found to be significantly lower when compared with non-invasive group. Protein carbonyl groups were remarkably higher in bladder cancer patients than in healthy controls. Patients with bladder cancer were demonstrated to have significantly lower levels of total thiol groups and protein-bound thiol groups as compared to healthy controls. Protein-bound thiol groups in patients with invasive bladder cancer revealed a more significant decline, than in non-invasive group.

Effect of alpha-lipoic acid on lipid peroxidation and anti-oxidant enzyme activities in diabetic rats.

1. Oxidative damage has been suggested to be a contributory factor in the development and complications of diabetes. Recently, alpha-lipoic acid (ALA) has gained considerable interest as an anti-oxidant. Various studies have indicated the anti- oxidant effects of ALA and its reduced form dihydrolipoic acid. Therefore, it appears that these compounds have important therapeutic potential in conditions where oxidative stress is involved. The aim of the present study was to investigate the effect of ALA supplementation on lipid peroxidation and anti-oxidant enzyme activities in various tissues in diabetic rats. 2. Male Wistar rats were divided into three groups. Diabetes was induced by streptozotocin (STZ) injection in the two groups of rats to be supplemented and not to be supplemented with ALA. Another group of rats, which received saline injection, formed the control group. After 5 weeks of diabetes, rats were killed. In order to assess the redox status of various organs in the diabetic and control rats, thiobarbituric acid-reactive substances (TBARS) and glutathione (GSH) levels, as well as superoxide dismutase (SOD), glutathione peroxidase (G-Px) and glutathione reductase (G-Red) activities were determined in the liver, pancreas and kidney. 3. In both diabetic groups, TBARS levels and SOD activity were increased in the liver and pancreas, G-Px and G-Red activities were increased in the kidney and GSH levels were decreased in all organs compared with controls. In the ALA- supplemented group, TBARS levels were decreased, GSH levels were increased in the liver and pancreas, SOD activity was decreased in the liver, G-Px activity remained unchanged in all tissues and G-Red activity was increased in the pancreas compared with the diabetic group that did not receive ALA supplementation. 4. In conclusion, ALA supplementation has disparate effects on the redox status of different organs. These data are not sufficient for confirmation the beneficial effects of ALA supplementation on the redox status of various organs in diabetic rats.

Postmenopausal hormone replacement therapy use decreases oxidative protein damage.

OBJECTIVES: The aim of this study is to evaluate oxidative protein damage (OPD) by investigating protein carbonyl (PCO) and nitrotyrosine (NT) levels, oxidative stress by total thiol (T-SH), erythrocyte glutathione (GSH) and nitric oxide (NO) levels in women receiving hormone replacement therapy (HRT). MATERIALS AND METHODS: To examine the influence of oxidative stress on OPD, we studied 12 postmenopausal women who had received HRT for 6 months, and 13 postmenopausal women who did not receive HRT, as the control group. All subjects were non-smokers. Blood samples were drawn in the fasting state and processed within 1 h of collection. For NT and NO, serum samples were stored at -70 degrees C until analysis; all other parameters were determined on the same day of collection. RESULTS: After 6 months, plasma PCO and T-SH levels were decreased, GSH and NO levels were increased, and NT levels were not changed in 12 postmenopausal women receiving HRT. Except the NT levels, the rest of the parameters did not significantly change in the control group. Interestingly, mean NT levels in the control group increased significantly. CONCLUSIONS: A crucial part of the protective effect of HRT on the cardiovascular system arises secondary to the interaction between estrogen and vessel wall. Our results suggest that an important component of the mechanism underlying this interaction may depend on estrogen's antioxidant effect and its preventive role in OPD.