Sebahat Ozdem

Erythrocyte, plasma, and serum antioxidant activities in untreated toxic multinodular goiter patients

Erythrocyte, plasma, and serum antioxidant activities were studied in patients with newly diagnosed and untreated toxic multinodular hyperthyroid goiter and compared to healthy control subjects. Erythrocyte antioxidant enzyme activities, glutathione, malondialdehyde, and ceruloplasmin levels were significantly increased, whereas serum vitamin E, plasma vitamin C, and selenium levels were decreased in hyperthyroid patients compared to control subjects. The findings show that untreated toxic multinodular goiter causes profound alterations in components of the antioxidant system in erythrocytes indicative of increased oxidative stress. Taken together, these data suggest that hyperthyroid patients may benefit from dietary supplements of antioxidants.

Experimental hyperhomocysteinemia disturbs bone metabolism in rats.

Objective. To investigate whether experimental hyperhomocysteinemia (HHCY) can induce adverse changes in bone metabolism. Methods. Blood and urine samples were collected from rats fed with a methionine‐enriched diet (HHCY, n = 18) or an isocaloric control diet (control, n = 10) for 12 weeks. Biochemical bone turnover markers (osteocalcin, hydroxyproline, N‐terminal collagen I telopeptides and homocysteine (HCY), folate and vitamin B12) were measured. Whole body bone mineral density (BMD) was assessed by dual energy X‐ray absorptiometry. Results. HCY was significantly higher in HHCY than in control rats (16.2 versus 3.2 µmol/L; p = 0.0006). Bone resorption parameters hydroxyproline (1.60±0.6 versus 0.85±0.4; p<0.05) and N‐terminal collagen I telopeptides (150.8±78 versus 48.1±26 nmol/L BCE; p<0.05) increased, whereas bone formation marker osteocalcin (9.01±3.8 versus 15.07±4.2 ng/mL; p<0.05) decreased in HHCY compared to control rats. The relation N‐terminal collagen I telopeptides/osteocalcin significantly increased in HHCY compared to control rats (13.14±3.1 versus 4.14±1.9). BMD measurement did not reveal any differences between groups. Conclusion. These findings demonstrate a significant modification of bone turnover in HHCY rats. The relation between bone resorption and formation indicates a shift toward bone resorption, which might be a plausible explanation for the relation between HHCY and fracture risk.

Insulin resistance in children with Helicobacter pylori infection

We aimed at investigating insulin resistance in children with Helicobacter pylori (H. pylori) infection. Fasting serum insulin and glucose levels were determined in 31 children with H. pylori (+) (H. pylori-infected group, 20 girls and 11 boys, median age 12 yr, range 6–17) and 29 H. pylori (−) (control group, 18 girls and 11 boys, median age 13 yr, range 5–16). Insulin resistance was assessed using homeostasis model assessment of insulin resistance (HOMA-IR) score. Fasting serum glucose levels did not differ significantly between H. pylori (+) and (−) children. Both HOMA-IR score and serum insulin levels were significantly higher in H. pylori-infected compared to control children. The findings of the present study suggested that there is a certain relation between H. pylori infection and insulin resistance in children.

Bone metabolism markers and bone mineral density in children with neurofibromatosis type-1

Some experimental studies suggested that there may be a bone formation defect rather than a disorder in bone resorption in patients NF1. The aim of this study was to determine bone mineral density (BMD) with dual-energy X-ray absorptiometry (DEXA) and investigate specific bone formation and bone resorption and bone turnover markers in children with NF1. Thirty-two children and adolescents (16 boys, 16 girls; 16 prepubertal, 16 pubertal) with NF1 were recruited. Their age ranged from 3 to 17 years. They were compared with matched healthy children. Dual-energy X-ray absorptiometry were applied to 26 patients and 27 controls. Nine of 32 subjects with NF1 had a skeletal abnormality. BMD of the lumbar spine, and femoral neck in NF1 patients significantly decreased compared to that of healthy subjects. They were also significantly decreased in pubertal patients when compared to pubertal controls and in prepubertal patients when compared to prepubertal controls. Patients with skeletal abnormalities were found to have significantly lower level of osteocalcin when compared to patients without skeletal abnormality. Other biochemical markers did not exhibit any difference between the groups. In conclusion, our findings suggest that bone formation markers rather than DEXA could be good predictors of skeletal abnormalities among NF1 patients. However, in our study the number of the NF1 patients with skeletal abnormality and the number of bone formation markers studied were all limited. It is appropriate to perform larger studies with other bone formation markers beside osteocalcin.

Effects of Propylthiouracil Treatment on Antioxidant Activities in Blood of Toxic Multinodular Goiter Patients

Erythrocyte, serum and plasma antioxidant activities and the effects of propylthiouracil (PTU) treatment on these activities were studied in patients with toxic multinodular goiter. The activities of the erythrocyte antioxidant enzymes (glucose-6-phosphate dehydrogenase, catalase, Cu/Zn-superoxide dismutase, selenium (Se)-dependent glutathione peroxidase and glutathione reductase) and the levels of erythrocyte Se, serum ceruloplasmin and plasma malondialdehyde were significantly higher while serum vitamin E, plasma vitamin C and plasma Se were lower in hyperthyroid patients. PTU treatment, not for 1 but for 3 months caused a partial reversal of antioxidant activities to euthyroid levels. It is suggested that alterations in blood antioxidant activities following PTU treatment might be due to the antioxidant and/or antithyroid effect of this drug.

Serum anti-Müllerian hormone levels do not predict the efficiency of testicular sperm retrieval in men with non-obstructive azoospermia

Background. We aimed to determine whether serum concentrations of anti-Müllerian hormone (AMH) can be used as a tool for prediction of the efficacy of sperm retrieval. Methods. This was a prospective cohort observational study. AMH levels were determined in 47 men presenting for infertility evaluation. Group 1 consisted of 24 infertile patients diagnosed with non-obstructive azoospermia. Group 1 was further divided into two subgroups. The patients with spermatozoa in their testicular samples constituted group 1a (n = 13), while the patients with absence of spermatozoa constituted group 1b (n = 11). Twenty-three normozoospermic fertile men constituted group 2. Serum AMH was measured before obtaining testicular specimens. Results. Testicular spermatozoa were recovered in 13 out of the 24 patients (54%). Demographic characteristics of the three groups were similar. The difference between serum AMH levels among the three groups did not reach statistical significance. Conclusions. We speculated that although AMH is secreted predominantly into the seminiferous tubules, studying serum samples might be more advantageous than seminal plasma because the presence of seminal proteases could influence AMH levels in the latter. However, our results did not demonstrate differences in serum concentrations of AMH between the studied groups. Studies with extended patient populations focusing on seminal plasma concentrations of AMH are warranted.

Comparison of TEST 1 with SRS 100 and ICSH reference method for the measurement of the length of sedimentation reaction in blood.

Abstract Background: We evaluated the measurement of length of sedimentation reaction in blood (LSRB) by TEST 1 and compared the results with those for the Westergren and Sed Rate Screener 100 (SRS 100) methods. Methods: LSRB was measured in 113 paired blood samples. Results: TEST 1 correlated significantly with the Westergren (r=0.94) and SRS 100 (r=0.90) methods with low bias (−0.29 and −1.92mm/h, respectively) and limits of agreement (−14.5 to 13.9, and −23.4 to 19.6mm/h, respectively). Hematocrit (Htc) correlated negatively with LSRB in TEST 1 (r=−0.54) and SRS 100 (r=−0.53) only in samples with high Htc (≥35%). The bias and limits of agreement between TEST 1 and Westergren in samples with low (−1.46 and −22.3 to 19.3mm/h) and high (0.43 and −7.29 to 8.14mm/h) Htc were comparable to those between SRS 100 and Westergren (1.83 and −27.2 to 30.9mm/h for low, 0.71 and −7.27 to 8.70mm/h for high Htc samples). Total protein and fibrinogen correlated similarly with LSRB in both TEST 1 (r=0.23 and 0.48, respectively) and SRS 100 (r=0.30 and 0.51, respectively). Conclusions: The findings suggested that TEST 1 is a reliable, precise and accurate system for measurement of LSRB in clinical laboratories with high workload.

Endogenous orexin-A modulates gastric motility by peripheral mechanisms in rats

Orexin-A (OXA) and orexin receptor type 1 (OX1R) are found in enteric nervous system and smooth muscle cells in the digestive tract. Fasting is a stimulant for OXA synthesis. The aim of the present study was to investigate central and peripheral effects of endogenous OXA on gastric motility. Endogenous OXA synthesis was induced by 36h fasting. Vagotomy was used to evaluate N.vagus-mediated effects of OXA. Gastric emptying and interdigestive gastric motility were measured by spectrophotometric and manometric methods, respectively. Rats were pretreated with OX1R antagonist SB-334867 prior to measurements. Plasma OXA concentration was assayed with radioimmunoassay while preproorexin (PPO) expression was determined with Western blotting in gastric and hypothalamic tissues. OXA immunoreactivity in antrum was determined with immunohistochemistry. Plasma OXA level, PPO protein expression and OXA immunoreactivity were significantly increased in response to 36h fasting. Endogenous OXA facilitated gastric emptying and inhibited gastric interdigestive motility. As these effects were abolished with SB-334867, it is likely that gastrokinetic effects of OXA are mediated via OX1R. Vagotomy did not alter OXA-mediated effects. According to current data, OXA is up-regulated both centrally and peripherally upon fasting. Endogenous OXA accelerates gastric emptying while it inhibits interdigestive motility.

Caffeic acid phenethyl ester modulates aflatoxin B1‐induced hepatotoxicity in rats

Aflatoxin B1 (AFB1) is the most potent of the mycotoxins and is widely observed in nutrition abnormalities. There are some studies suggesting oxidative stress‐induced toxic changes on liver related to AFB1 toxicity. The aim of the present study was to evaluate whether antioxidant caffeic acid phenethyl ester (CAPE) relieves oxidative stress in AFB1‐induced liver injury in rat. Twenty‐four male rats were equally divided into three groups. The first group was used as a control. The second group received three doses of AFB1. The three doses of CAPE were given to constitute the third group with doses of AFB1. After 10 days of experiment, liver and serum samples were taken from all animals. Serum gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), glutathione s‐transferase (GST), nitric oxide (NO) and sulfhydryl values were higher in the AFB1 group than in control, whereas serum GGT, ALP, GST and NO values were decreased by in the AFB1 + CAPE group than in AFB1 group. Liver GST, total oxidant capacity, sulfhydryl, apoptosis index and ischemia‐modified albumin values were higher in the AFB1 group than in control, whereas the GST activity and apoptosis index were lower in the AFB1 + CAPE group than in the AFB1 group. There were histopathological degeneration and apoptosis in hepatocytes of AFB1 group. The findings were totally recovered by CAPE administration. In conclusion, we observed that AFB1 caused oxidative and nitrosative hepatoxicity to hepatocytes in the rat. However, CAPE induced protective effects on the AFB1‐induced hepatoxicity by modulating free radical production, biochemical values and histopathological alterations. Copyright

Plasma homocysteine levels in patients with β‐thalassaemia major

Objective. We investigated the level of homocysteine (HCY) and its relation with vitamin B12, folate and oxidative stress in patients with β‐thalassaemia major. Material and methods. Plasma HCY, methionine, advanced oxidation protein products (AOPP) and serum vitamin B12, folate, ferritin and total antioxidant capacity (TAC) were determined in 32 thalassaemic patients and 27 control subjects. Results. HCY (6.44±0.44 versus 8.71±0.57 µmol/L), methionine (12.57±1.8 versus 22.2±3.8 µmol/L), folate (9.14±0.48 versus 15.38±0.71 nmol/L) and TAC (0.34±0.03 versus 0.56±0.03 mmol/L) significantly decreased in thalassaemic patients, whereas AOPP (20.26±1.8 versus 11.30±0.2 μmol/L) and ferritin (3481.0±512 versus 46.9±4.6 ng/mL) significantly increased. Vitamin B12 levels were similar in both groups (259.1±16.6 versus 228.9±7.4 pmol/L). Conclusions. These findings suggest that increased and uncompensated oxidative stress may lead to an increment in HCY catabolism in thalassaemic patients.