Serum macroprolactin levels in pregnancy and association with thyroid autoimmunity.

BACGROUND: To assess the contribution of macroprolactin to high serum prolactin levels and their association with thyroid status and thyroid autoimmunity during pregnancy. METHODS: 138 pregnant women who suspected of having thyroid dysfunction were studied and divided into three groups according to the thyroid status; group 1; euthyroidism (n 40), group 2; hypothyroidism (n 54), and group 3; hyperthyroid (n 44). Polyethylene glycol (PEG) precipitation method was used for detection of macroprolactin. A percentage recovery of 40 % or less is considered as macroprolactinemia. If macroprolactin was negative, the percentage of monomeric prolactin recovery (monoPRL %) after PEG precipitation was used for comparison between the groups. RESULTS: Macroprolactinemia was found in two patients (1.4 %) one from hypothyroid and other from euthyroid group. Basal prolactin levels in these patients were 400 and 403 ng/mL respectively. Referring to all patients, there was no correlation between PRL, macroPRL or monoPRL % with thyroid hormone status and also with the serum levels of thyroid antibodies (p > 0.05). A positive correlation was observed between the serum levels of PRL with TSH (p = 0.014 and r = 0.219), while a negative correlation was found with FT4 (p = 0.011 and r = -0.227). CONCLUSIONS: Despite the fact that serum prolactin levels were found to be high during pregnancy, the contribution of macroprolactin was found to be insignificant in our study. Unlike other auto immune diseases, we could not find any relationship between thyroid autoimmunity and PRL, macroPRL or monoPRL %. These results confirmed that measured prolactin was quite homogeneous during pregnancy.

Obstructive sleep apnea causes oxidative damage to plasma lipids and proteins and decreases adiponectin levels.

UNLABELLED: PUPOSE: Obstructive sleep apnea (OSA) is associated with various metabolic disorders, and oxidative stress was suggested to play an important role. In the present study, we aimed to investigate serum adiponectin and oxidative stress markers, especially protein carbonyls, and to evaluate the correlation between these parameters and lipid, insulin and fasting glucose concentrations in OSA patients and controls. METHOD: Blood was drawn from healthy male volunteers following full-night polysomnographic evaluation. Subjects were classified as controls (n = 24), mild OSA group (n = 9) and moderate-severe OSA group (n = 17) according to their apnea-hypopnea indices (AHIs). Serum lipids, fasting glucose, adiponectin, malondialdehyde (MDA), protein carbonyl concentrations, and paraoxonase activities were measured in all subjects. RESULTS: Results of this study indicated that serum adiponectin concentrations were significantly decreased and MDA and protein carbonyl concentrations were significantly elevated in OSA patients compared to the controls. Protein carbonyl and MDA concentrations were significantly and positively correlated with AHI, while a significant negative correlation was found between adiponectin concentrations and AHI. Adiponectin levels were negatively correlated with MDA levels. CONCLUSION: Results of this study, which is the first human study investigating and describing serum protein carbonyl concentrations in OSA patients, reveal that OSA causes increments in oxidative damage and decreases adiponectin levels. The recurrent hypoxia-reoxygenation attacks in OSA patients may activate oxidative stress, elevating sympathetic activity and leading to low levels of adiponectin.

Effects of hypoxic preconditioning in antioxidant enzyme activities in hypoxic-ischemic brain damage in immature rats.

AIM: HI (hypoxic-ischemic) brain injury is a major cause of neonatal mortality and longterm neurological morbidity. The aim of the present study was to investigate the effects of HPC (hypoxic preconditioning) on the oxidative-antioxidative status in the neonatal HI brain model. MATERIAL AND METHODS: Fifty five 7-day-old rats were placed into; Control, HPC, HPC+HI insult, and HI insult groups. HPC, The HPC+HI insult groups were subjected to hypoxia (37 degrees C, 8%O2) and the control group to normoxia for 2.5 hrs. Twenty-four hours later, the rats in the HPC+HI insult and HI insult groups were exposed to cerebral HI produced by unilateral right common carotid artery (CCA) occlusion combined with 90 min hypoxia. Four hours after recovery, the malondialdehyde (MDA) level and the activities of superoxide dismutase (SOD), and glutathione peroxidase (GPx) were determined in the brain tissues of the rats. RESULTS: The findings of the present study suggest increased lipid peroxidation and/or decreased antioxidant activity in the brain of the HI rats. CONCLUSION: The beneficial effects of HPC might not be related to the alterations in the antioxidative activity.

Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative-antioxidative systems.

OBJECTIVE: The aim of the present study was to investigate the oxidative-antioxidative systems and effects of different antidepressants on these systems in patients with major depressive disorder (MDD). METHOD: Ninety-six patients with a Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV) diagnosis of MDD and 54 healthy controls were included in the study. Plasma malondialdehyde (MDA) levels and susceptibility of red blood cells (RBCs) to oxidation were determined to investigate the oxidative status, plasma vitamin E, vitamin C, serum total carotenoid levels, total antioxidant capacity (TAOC), RBC superoxide dismutase (SOD) and whole blood glutathione peroxidase (GPx) activities were measured to investigate the antioxidative defence before and after 6 weeks of antidepressant treatment. RESULTS: Plasma MDA levels and susceptibility of RBCs to oxidation were significantly higher in the MDD group compared with the control group. RBC SOD activity was significantly increased in patients with MDD, and furthermore there was a significant positive correlation between the severity of the disease and SOD activity. CONCLUSION: MDD is accompanied with oxidative stress; however, oxidative-antioxidative systems do not seem to be affected by 6 weeks of antidepressant treatment.