A new approach to an old hypothesis; phototherapy does not affect ductal patency via PGE2 and PGI2.

OBJECTIVE: Numerous investigations have demonstrated that phototherapy (PT) directly or indirectly causes ductal patency by photorelaxation effect. In this observational study, we aimed to assess the effect of PT on the incidence of patent ductus arteriosus (PDA) together with prostaglandins (PGE2) and (PGI2) levels in preterm infants. METHODS: Preterm infants whose gestational age<34 weeks and who required PT in the first 3 d of life were enrolled in this prospective study. The clinical signs of PDA, the data of detailed echocardiographic study were recorded and plasma PGE2 and PGI2 levels were measured before and after PT. The outcome measures were the status of ductus arteriosus and alterations of PGE2 and PGI2 levels under the effect of PT. RESULTS: A total of 44 preterm infants were enrolled in the study, of these 21 (47.7%) were in Group 1 (Non-PDA Group) and 23 (52.3%) were in Group 2 (PDA Group). After PT, ductal reopening occurred in three infants (14.3%) in Group 1, while ductus closed in four infants in Group 2 (17.3%). PT does not seem to effect ductal patency for both groups (p=0.250 and p=0.125, respectively). PGE2 levels were not different before and after PT for both groups (p=0.087, p=0.408, respectively). However, PGI2 levels were significantly decreased after PT in both groups (p=0.006, and p=0.003, respectively). CONCLUSION: There was no effect of PT on ductal patency. We can conclude that PGs were eliminated simultaneously with ductal closure and photorelaxation effect did not influence PG levels.

Serum aflatoxin levels of the healthy adult population living in the north and south regions of Turkey.

OBJECTIVE: To determine the serum concentrations of aflatoxin B1 (AFB1), aflatoxin B2 (AFB2), aflatoxin G1 (AFG1) and aflatoxin G2 (AFG2) in the healthy adult population living in both the Black Sea and Mediterranean regions of Turkey and to investigate the regional, seasonal and gender variability in aflatoxins (AF) exposure in these regions. DESIGN: Serum AFB1, AFB2, AFG1 and AFG2 concentrations were analysed by HPLC. Settings In total, four hundred and eighty-four serum samples were analysed. SUBJECTS: Four hundred and eighty-four healthy adult volunteers living in rural areas of the Black Sea and Mediterranean regions of Turkey were studied. RESULTS: The mean serum concentration of total AF in the Black Sea region was 1·33 ppb (min-max 0·15-3·38 ppb) and 0·90 ppb (min-max 0·18-2·48 ppb) for summer and winter, respectively. In the Mediterranean region, the mean serum concentration of total AF was determined as 0·55 ppb (range 0·04-1·72 ppb) for summer and 0·45 ppb (range 0·12-1·43 ppb) for winter. The total AF concentrations in serum samples were statistically higher in summer compared with winter for the two regions. The differences between the regions were statistically significant concerning all samples, with higher total AF concentrations in the Black Sea region. CONCLUSIONS: The overall results suggest that the Turkish population living in these two regions is continuously exposed to AF, particularly in the summer, and that mycotoxin contamination in food should be monitored routinely for food safety and human health.

The effects of di(2-ethylhexyl)phthalate on rat liver in relation to selenium status.

This study was performed to determine the hepatotoxicity of di(2-ethylhexyl)phthalate (DEHP) in relation to selenium status. In 3-week-old Sprague-Dawley rats, selenium deficiency was induced by a ≤0.05 selenium mg/kg. A selenium supplementation group was given 1 mg selenium/kg diet for 5 weeks. Di(2-ethylhexyl)phthalate-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the experiment. Histopathology, peroxisome proliferation, catalase (CAT) immunoreactivity and activity and apoptosis were assessed. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR1)], superoxide dismutase (SOD), and glutathione S-transferase (GST); aminotransferase, total glutathione (tGSH), and lipid peroxidation (LP) levels were measured. Di(2-ethylhexyl)phthalate caused cellular disorganization while necrosis and inflammatory cell infiltration were observed in Se-deficient DEHP group (DEHP/SeD). Catalase activity and immunoreactivity were increased in all DEHP-treated groups. Glutathione peroxidase 1 and GPx4 activities decreased significantly in DEHP and DEHP/SeD groups, while GST activities decreased in all DEHP-exposed groups. Thioredoxin reductase activity increased in DEHP and DEHP/SeS, while total SOD activities increased in all DEHP-treated groups. Lipid peroxidation levels increased significantly in SeD (26%), DEHP (38%) and DEHP/SeD (71%) groups. Selenium supplementation partially ameliorated DEHP-induced hepatotoxicity; while in DEHP/SeD group, drastic changes in hepatic histopathology and oxidative stress parameters were observed.

Effects of di(2-ethylhexyl)phthalate on testicular oxidant/antioxidant status in selenium-deficient and selenium-supplemented rats.

Di(ethylhexyl)phthalate (DEHP), the most widely used plasticizer, was investigated to determine whether an oxidative stress process was one of the underlying mechanisms for its testicular toxicity potential. To evaluate the effects of selenium (Se), status on the toxicity of DEHP was further objective of this study, as Se is known to play a critical role in testis and in the modulation of intracellular redox equilibrium. Se deficiency was produced in 3-weeks-old Sprague-Dawley rats feeding them ≤0.05 mg Se /kg diet for 5 weeks, and Se-supplementation group was on 1 mg Se/kg diet. DEHP-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), and thus the GSH/GSSG redox ratio; and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP was found to induce oxidative stress in rat testis, as evidenced by significant decrease in GSH/GSSG redox ratio (>10-fold) and marked increase in TBARS levels, and its effects were more pronounced in Se-deficient rats with ∼18.5-fold decrease in GSH/GSSG redox ratio and a significant decrease in GPx4 activity, whereas Se supplementation was protective by providing substantial elevation of redox ratio and reducing the lipid peroxidation. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting testicular tissue from the oxidant stressor activity of DEHP.

Selenium levels, selenoenzyme activities and oxidant/antioxidant parameters in H1N1-infected children.

Selenium (Se) is an essential trace element, and it shows its biological functions within low molecular Se compounds and Se-containing proteins, known as "selenoproteins". Glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs) are the most important selenoproteins functioning as antioxidant enzymes. These enzymes protect the body from the endogenous products of cellular metabolism that have been implicated in DNA damage, mutagenesis, and carcinogenesis. H1N1 virus is a subtype of the influenza A virus and was an endemic in humans in 2009 and 2010. Taking into account the high incidence of Se deficiency and the high mortality and morbidity rates in H1N1 infection, this study was designed to investigate the plasma and erythrocyte Se levels, selenoenzyme activities and other oxidant/antioxidant parameters in H1N1-infected children during the 2009-2010 pandemic. We observed a significant increase in C-reactive protein levels (245%) and marked decreases in both plasma and erythrocyte Se levels (11%, both) and in GPx1 (45%), GPx3 (16%) and TrxR (30%) activities in H1N1-infected children compared to the control group. In addition, significant decreases were observed in erythrocyte catalase (CAT) (38%), total superoxide dismutase (SOD) (42%) and glutathione S-transferase (GST) (19%) activities and in erythrocyte total glutathione (GSH) (18%) and plasma GSH (10%) concentrations, while marked increases were observed in plasma lipid peroxidation levels (27%). However, we did not find a significant difference in selenoprotein P (SePP) levels between the groups. Our findings show that Se-dependent and -independent blood redox systems are down-regulated in H1N1 influenza. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in infections, particularly in H1N1 influenza.

The carotenoid lycopene protects rats against DNA damage induced by Ochratoxin A.

Ochratoxin A (OTA), one of the most prevalent mycotoxins in the world, has nephrotoxic and hepatotoxic properties. Lycopene is an important carotenoid and has a high singlet-oxygen and free-radical scavenging capacity. This study was designed to investigate the possible protective effects of lycopene against the genotoxicity of OTA in rat tissues using the alkaline comet assay. Male Sprague-Dawley rats were used in the experiments. OTA (0.5 mg/kg b.w./day) was administered by gavage for 14 days, whereas lycopene was applied on the last 7 days or for 14 days of the feeding period, with OTA treatment. OTA caused marked increases in tail length, tail moment, and tail intensity vs. control both in the kidney and liver cells, but not in the lymphocytes. Lycopene administration alone for 7 and 14 days did not provide any significant change in DNA damage of the lymphocytes, renal and hepatic cells vs. controls. However, lycopene for both 7 and 14 days, with OTA exposure in renal and hepatic cells, supplied significant decreases in tail length, tail moment, and tail intensity vs. OTA-exposed rats. The effect of 14 days supplementation seemed to be more protective, particularly against hepatic cells. These results suggest that lycopene may protect hepatic and renal tissue from OTA-induced DNA damage.

Protective effect of lycopene against ochratoxin A induced renal oxidative stress and apoptosis in rats.

This study was designed to investigate the possible protective effect of lycopene against the renal toxic effects of OTA. Male Sprague-Dawley rats (<200 g, n=6) were treated with OTA (0.5 mg/kg/day) and/or lycopene (5 mg/kg/day) by gavage for 14 days. Histopathological examinations were performed and apoptotic cell death in both cortex and medulla was evaluated by TUNEL assay. Besides, biochemical parameters and activities of renal antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD); concentrations of total glutathione (GSH), and malondialdehyde (MDA) levels were measured. OTA treatment was found to induce oxidative stress in rat kidney, as evidenced by marked decreases in CAT (35%) activity and GSH levels (44%) as well as increase in SOD activity (22%) vs control group. Furthermore, TUNEL analysis revealed a significant increase in the number of TUNEL-positive cells in cortex (49%) and medulla (75%) in OTA administrated group compared to control (p<0.05). Lycopene supplementation with OTA increased GPx1 activity and GSH levels, and decreased apoptotic cell death in both cortex and medulla vs. control. The results of this study showed that at least one of the mechanisms underlying the renal toxicity of OTA is oxidative stress and apoptosis is the major form of cell death caused by OTA. Besides, our data indicate that the natural antioxidant lycopene might be partially protective against OTA-induced nephrotoxicity and oxidative stress in rat.

Thyroidal effects of di-(2-ethylhexyl) phthalate in rats of different selenium status.

This study was designed to investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) on thyroid hormone levels and oxidant/antioxidant parameters in the rat and to evaluate the effects of selenium status. Selenium deficiency was produced by feeding 3-week-old Sprague-Dawley rats with <0.05 mg selenium/kg body weight for 5 weeks, and the supplementation group received a diet of 1 mg selenium/kg body weight. DEHP-treated groups received the compound at a dose of 1000 mg/kg by gavage during the last 10 days of the feeding period. Levels of thyroid hormone levels as well as selenoenzyme (glutathione peroxidase 1, thioredoxin reductase), catalase, and superoxide dismutase (SOD) activity and thiobarbituric acid reactive substance (TBARS) were measured. Total thyroxine (TT4) levels decreased significantly with DEHP exposure (~25%), whereas TT3 level was not altered. The TT4 lowering effect of DEHP exposure was not affected by selenium deficiency but was observed when animals exposed to DEHP received a selenium supplement. DEHP was found to alter the antioxidant status and induce oxidative stress in rat thyroid by increasing SOD activity (~30%) and TBARS levels (~35%). The effects of DEHP were much more pronounced in selenium-deficient rats, as evidenced by significant increases in SOD activity (~65%) and TBARS levels (~55%) compared with the control levels. Thus, these results show the thyroid-disrupting effect of DEHP in rats and protection by selenium.

Di(2-ethylhexyl)phthalate-induced renal oxidative stress in rats and protective effect of selenium.

This study was designed to examine the oxidative stress potential of di(2-ethylhexyl)phthalate (DEHP) on rat kidney and to evaluate possible protective effect of selenium (Se) status. Se deficiency (SeD) was produced in 3-week old Sprague-Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks; Se supplementation group (SeS) was on 1 mg Se/kg diet. DEHP treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of total glutathione (GSH), thiols and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP treatment was found to induce oxidative stress in rat kidney, as evidenced by significant decreases in GPx1 (~20%) and SOD (~30%) activities and GSH levels (~20%), along with marked decrease in thiol content (~40%) and increase in TBARS (~30%) levels. The effects of DEHP was more pronounced in SeD rats, whereas Se supplementation was protective by providing substantial elevations of GPx1 and GPx4 activities and GSH levels. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting renal tissue from the oxidant stressor activity of DEHP.

Selenium and/or iodine deficiency alters hepatic xenobiotic metabolizing enzyme activities in rats.

The objective of this study was to investigate the effects of iodine (I(2)) and/or selenium (Se) deficiency on thyroid hormones and hepatic xenobiotic metabolizing enzyme systems using a triple animal model. Three-week-old male Wistar rats were fed for seven weeks. Se deficiency was introduced by a diet containing <0.005 mg/kg Se, and I(2) deficiency was produced by sodium perchlorate containing drinking water. The levels of plasma thyroid hormones [total T(4) (TT(4)), total T(3) (TT(3))], thyroid stimulating hormone (TSH); total microsomal cytochrome P450 (CYP450) and cytochrome b5 (CYP b5) levels; activities of microsomal NADPH-cytochrome P450 reductase (P450R), microsomal aniline hydroxylase (CYP2E1), microsomal 7-ethoxyresorufin O-deethylase (EROD), microsomal 7-pentoxyresorufin O-depentylase (PROD) and cytosolic glutathione S-transferase (GST) were determined. In I(2) deficiency total CYP450 levels, activities of CYP2E1, EROD and GST decreased, and CYP b5 content increased significantly. In Se-deficient rats, total CYP450 level and CYP2E1 activity increased, and EROD and GST activities and CYP b5 level decreased significantly. In combined I(2) and Se deficiency, except for CYP450 content and CYP2E1 activity, all enzyme activities and CYP b5 content decreased significantly compared to control group. Overall results of this study have suggested that metabolism of xenobiotics as well as endogenous compounds is affected by Se and I(2) status.

The effects of di(2-ethylhexyl)phthalate exposure and selenium nutrition on sertoli cell vimentin structure and germ-cell apoptosis in rat testis.

This study aimed to investigate the effects of di(2-ethylhexyl)phthalate (DEHP) on Sertoli-cell vimentin filaments and germ-cell apoptosis in testes of pubertal rats at different selenium (Se) status. Se deficiency was produced in 3-weeks old Sprague-Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks, Se supplementation group was on 1 mg Se/kg diet, and DEHP was applied at 1000 mg/kg dose by gavage during the last 10 days of the feeding period. The diet with excess Se did not cause any appreciable alteration in vimentin staining and apoptosis of germ cells, but Se deficiency caused a mild decrease in the intensity of vimentin immunoreactivity and enhanced germ-cell apoptosis significantly (approximately 3-fold, p <0.0033). DEHP exposure caused disruption and collapse of vimentin filaments and significantly induced apoptotic death of germ cells (approximately 8-fold, p <0.0033). In DEHP-exposed Se-deficient animals, compared with the control, collapse of vimentin filaments was more prominent; there was serious damage to the seminiferous epithelium; and a high increment (approximately 25-fold, p <0.0033) in apoptotic germ cells was observed. Thus, Se deficiency exacerbated the toxicity of DEHP on Sertoli cells and spermatogenesis, whereas Se supplementation provided protection. These results put forward the critical role of Se in the modulation of redox status of testicular cells and emphasize the importance of Se status for reproductive health.

Reproductive toxicity of di(2-ethylhexyl) phthalate in selenium-supplemented and selenium-deficient rats.

Phthalates are abundantly produced plasticizers, and di(ethylhexyl) phthalate (DEHP) is the most widely used derivative in various consumer products and medical devices. Animal studies show that DEHP and various other phthalates cause reproductive and developmental toxicity. Although the evidences are limited, it seems reasonable that DEHP may have a potential for similar adverse effects in humans. Such concerns are increasing, particularly for the developing reproductive system of male infants and children. By taking into account the essentiality of selenium (Se) in testicular structure and functions and the high prevalence of inadequate Se intake in various part of the world, this study was designed to investigate the testicular toxicity of DEHP in Se-deficient male rats and to examine the possible preventive effects of Se supplementation on phthalate toxicity. Se deficiency was generated by feeding 3-week-old Sprague-Dawley rats with a ≤0.05 Se mg/kg diet for 5 weeks. Supplementation groups were on a 1 mg Se/kg diet, and DEHP-treated groups received a 1,000 mg/kg dose by gavage during the last 10 days of the feeding period. Testicular histopathology, sperm count and motility, and sperm morphology were examined, and plasma levels of sex hormones were measured. Toxicity and antiandrogenic effects of DEHP were evidenced by disturbed testicular histology and spermatogenesis, diminished testosterone, leutinizing hormone (LH) and follicle stimulating hormone (FSH) levels, and sperm motility. The effects of DEHP were much more pronounced in Se-deficient rats, whereas Se supplementation was found to be protective, reflecting its regulating role in cellular redox equilibrium.

Fenvalerate induced hepatic oxidative stress in selenium- and/or iodine-deficient rats.

Considering the potential adverse effects of selenium and iodine deficiencies, and frequency of intensive but improper use of insecticides, this study was designed to evaluate the effects of a pyrethroid insecticide, fenvalerate, on the oxidant/antioxidant status of liver using a rat model of iodine and/or selenium deficiency. The study was conducted on eight groups of 3-week old Wistar rats. Iodine and/or selenium deficiency was introduced by feeding the animals with a diet containing <0.005 mg selenium/kg and/or supplying with 1% sodium perchlorate containing drinking water for a period of 7 weeks. Fenvalerate exposure (100 mg/kg/d, i.p., for the last 7 days) in normal rats increased hepatic glutathione peroxidase activity and lipid peroxidation, decreased glutathione content, but did not change the activities of catalase or any of the superoxide dismutase forms; in iodine-deficient animals caused only the elevation of lipid peroxidation; in selenium-deficient animals and in combined iodine/selenium deficiency decreased glutathione peroxidase, increased catalase activities and lipid peroxidation, and decreased all the forms of superoxide dismutase activity only in combined deficiency. These results suggested that fenvalerate is an oxidant stress inducer in rat liver, and its potential effects on pro-oxidant/antioxidant balance may also be important for human populations, particularly with iodine and/or selenium deficiencies.

Evaluation of cytotoxicity and oxidative DNA damaging effects of di(2-ethylhexyl)-phthalate (DEHP) and mono(2-ethylhexyl)-phthalate (MEHP) on MA-10 Leydig cells and protection by selenium.

Di(2-ethylhexyl)-phthalate (DEHP) is the most abundantly used phthalate derivative, inevitable environmental exposure of which is suspected to contribute to the increasing incidence of testicular dysgenesis syndrome in humans. Oxidative stress and mitochondrial dysfunction in germ cells are suggested to contribute to phthalate-induced disruption of spermatogenesis in rodents, and Leydig cells are one of the main targets of phthalates' testicular toxicity. Selenium is known to be involved in the modulation of intracellular redox equilibrium, and plays a critical role in testis, sperm, and reproduction. This study was aimed to investigate the oxidative stress potential of DEHP and its consequences in testicular cells, and examine the possible protective effects of selenium using the MA-10 mouse Leydig tumor cell line as a model. In the presence and absence of selenium compounds [30 nM sodium selenite (SS), and 10 µM selenomethionine (SM)], the effects of exposure to DEHP and its main metabolite mono(2-ethylhexyl)-phthalate (MEHP) on the cell viability, enzymatic and non-enzymatic antioxidant status, ROS production, p53 expression, and DNA damage by alkaline Comet assay were investigated. The overall results of this study demonstrated the cytotoxicity and genotoxicity potential of DEHP, where MEHP was found to be more potent than the parent compound. SS and SM produced almost the same level of protection against antioxidant status modifying effects, ROS and p53 inducing potentials, and DNA damaging effects of the two phthalate derivatives. It was thus shown that DEHP produced oxidative stress in MA-10 cells, and selenium supplementation appeared to be an effective redox regulator in the experimental conditions used in this study, emphasizing the critical importance of the appropriate selenium status.

Protective effect of selenium supplementation on the genotoxicity of di(2-ethylhexyl)phthalate and mono(2-ethylhexyl)phthalate treatment in LNCaP cells.

Selenium is an essential cofactor in the key enzymes involved in cellular antioxidant defense. It plays a critical role in testis and reproduction and regulates DNA damage within the prostate. Phthalates are ubiquitous environmental contaminants that cause alterations in endocrine and spermatogenic functions in animals. The objective of this study was to investigate the cytotoxicity and genotoxicity potentials of di(2-ethylhexyl)phthalate (DEHP), the most widely used phthalate and its primary toxic metabolite mono(2-ethylhexyl)phthalate (MEHP), and their effects on the antioxidant balance in the LNCaP human prostate adenocarcinoma cell line. Protection by selenium supplementation with either sodium selenite (SS, 30 nM) or selenomethionine (SM, 10 microM) was also investigated. Both DEHP (3mM) and MEHP (3 microM) caused significant decreases in cell viability; altered antioxidant status, particularly decreasing the GPx1 activity; and induced DNA damage as measured by the alkaline comet assay. Selenium supplementation was highly protective against cytotoxicity, partially prevented genotoxicity, and restored the antioxidant status. The results of this study suggested that the underlying mechanism of cytotoxicity and resulting disturbances produced by DEHP or MEHP was an an oxidative stress process and/or an effect on the expression of antioxidant enzymes, and accentuated the importance of selenium status, particularly with respect to the high probability of phthalate exposures and their adverse effects.

Trace elements status in multinodular goiter.

Importance of iodine and selenium in thyroid metabolism is well known, but the roles of other essential trace elements including copper, zinc, manganese and iron on thyroid hormone homeostasis remain unclear. The aim of this study was to investigate the status of those trace elements in benign thyroid diseases and evaluate possible links between trace element concentrations and thyroid hormones. The study group was composed of 25 patients with multinodular goiter. Concentrations of thyroid hormones (plasma-free thyroxine, FT(4); free triiodothyronine, FT(3); and thyrotropin, TSH), selenium, copper, zinc, manganese and iron in plasma, and urinary iodine were determined. The results were compared with those of a healthy control group (n=20) with no thyroid disorder. A mild iodine deficiency was observed in the patients with multinodular goiter whereas urinary iodine levels were in the range of "normal" values in healthy controls. All patients were euthyroid, and their thyroid hormone concentrations were not significantly different from the control group. Plasma selenium, zinc and iron concentrations did not differ from controls, while copper and manganese levels were found to be significantly higher in the patients with multinodular goiter indicating links between these trace elements and thyroid function and possibly in development of goiter. Besides iodine, there was a significant correlation between plasma copper concentration and FT(3)/FT(4) ratio.

Fenvalerate exposure alters thyroid hormone status in selenium- and/or iodine-deficient rats.

Considering the potential adverse effects of selenium and iodine deficiencies, and taking into account the widespread but often careless use of pyrethroid insecticides and their possible endocrine-disrupting effects, this study was undertaken to investigate the effects of fenvalerate on thyroid hormone parameters in both healthy and selenium- and/or iodine-deficient rats. Fenvalerate exposure had no effect on the TT4 levels of healthy controls but caused significant increases both in iodine deficiency (ID) and selenium plus iodine deficiency (ISeD), and a significant decrease in selenium deficiency (SeD). Dramatic increases in TT3 of all groups were observed by fenvalerate. Moreover, it caused insignificant decrease of thyroid stimulating hormone in healthy controls, no effect in SeD, and significant elevation in ID and ISeD. These results, thus, showed that the widely used pyrethroid insecticide fenvalerate has the potential to change significantly thyroid hormone parameters both in normal and deficiency states, and consequences of its thyroid status modifying effect might be of critical importance particularly in sensitive individuals and patients with thyroid dysfunction.

Determination of seasonal variations in serum ochratoxin A levels in healthy population living in some regions of Turkey by enzyme-linked immunosorbent assay.

This study has been undertaken to investigate the regional and seasonal variability in ochratoxin A (OTA) exposure of healthy population living in Black Sea and Mediterranean regions of Turkey by measuring serum OTA concentrations. The mean serum concentrations of OTA were determined to be 0.137 ng/mL (0.0306-0.887 ng/mL) and 0.312 ng/mL (0.028-1.496 ng/mL) in all samples for winter and summer, respectively by enzyme-linked immunosorbent assay (ELISA). The differences between mean values of OTA in all serum samples collected in summer and winter were statistically significant. The highest OTA concentration was determined in the children living in Black Sea Region in summer. The mean daily intake levels of OTA in all samples were estimated as 0.182 ng/kg b.w./day and 0.408 ng/kg b.w./day in winter and summer, respectively. The results showed that the mean serum concentrations of OTA in healthy population in both regions were found not to be exceeded 1 ng/mL in agreement with the distribution reported in most European countries and that the daily intake levels of OTA were calculated below the tolerable daily intake levels given by regulatory authorities. However, overall results suggest that Turkish population living in these regions is continuously exposed to OTA and that the exposure levels are also elevated in summer period compared to winter.

Plasma phthalate levels in pubertal gynecomastia.

OBJECTIVE: Several untoward health effects of phthalates, which are a group of industrial chemicals with many commercial uses including personal-care products and plastic materials, have been defined. The most commonly used, di-(2-ethylhexyl)-phthalate (DEHP), is known to have antiandrogenic or estrogenic effects or both. Mono-(2-ethylhexyl)-phthalate (MEHP) is the main metabolite of DEHP. In this study, we aimed to determine the plasma DEHP and MEHP levels in pubertal gynecomastia cases. PATIENTS AND METHODS: The study group comprised 40 newly diagnosed pubertal gynecomastia cases who were admitted to Hacettepe University Ihsan Dogramaci Children's Hospital. The control group comprised 21 age-matched children without gynecomastia or other endocrinologic disorder. Plasma DEHP and MEHP levels were measured by using high-performance liquid chromatography. Serum hormone levels were determined in some pubertal gynecomastia cases according to the physician's evaluation. RESULTS: Plasma DEHP and MEHP levels were found to be statistically significantly higher in the pubertal gynecomastia group compared with the control group (P < .001) (DEHP, 4.66 +/- 1.58 and 3.09 +/- 0.90 microg/mL, respectively [odds ratio: 2.77 (95% confidence interval: 1.48-5.21)]; MEHP, 3.19 +/- 1.41 and 1.37 +/- 0.36 microg/mL [odds ratio: 24.76 (95% confidence interval: 3.5-172.6)]). There was a statistically significant correlation between plasma DEHP and MEHP levels (r: 0.58; P < .001). In the pubertal gynecomastia group, no correlation could be determined between plasma DEHP and MEHP levels and any of the hormone levels. CONCLUSIONS: DEHP, which has antiandrogenic or estrogenic effects, may be an etiologic factor in pubertal gynecomastia. These results may pioneer larger-scale studies on the etiologic role of DEHP in pubertal gynecomastia.

Determination of ochratoxin A and total aflatoxin levels in corn samples from Turkey by enzyme-linked immunosorbent assay.

Forty-seven samples of corn were collected from various street bazaars and market outlets in different regions of Turkey and total aflatoxin (AF) and ochratoxin A (OTA) levels were determined by enzyme-linked immunosorbent assay (ELISA) following sample preparation. Levels of AF and OTA in corn samples ranged between 1.75-120.3 µg/kg and 1.08-8.57 µg/kg, respectively. Although 53% of the samples analysed had no detectable levels of AF, 4% of similar samples were found to contain AFs above the acceptable limit of 10 µg/kg in Turkey. For OTA, 4% of the corn samples had levels above the acceptable limit (3 µg/kg) in Turkey, with over 43% samples not found to contain this mycotoxin. Although the levels of mycotoxins analysed in this study were not found to be high and the percentage of samples contaminated above permitted limits were low, the importance of overall daily dietary intake should not be underestimated and control of these fungal metabolites in corn must be explored to minimise the hazards they may cause in humans.