Bisphenol derivatives in cord blood and association between thyroid hormones and potential exposure sources.

Endocrine-disrupting environmental chemicals are a public health concern, particularly fetal exposure to Bisphenol derivatives. This study aimed to assess fetal exposure to Bisphenol derivatives (BPA, BPF, and BPS) by measuring their levels in cord blood and investigating their association with plastic material used in daily life as well as cord blood TSH and free L-thyroxine (fT4) levels. In this descriptive study, a questionnaire with a face-to-face interview was administered before birth, and cord blood samples were taken immediately after delivery. The mean levels of BPA, BPF, TSH, and fT4 were measured as 10.69 ± 2.39 ng/ml, 3.80 ± 0.58 ng/ml; 2.36 ± 0.23 µIU/ml, and 14.18 ± 0.53 pg/ml, respectively, in a total of 104 cord blood samples. All BPS levels remained below the detection limit. Linear regression analysis revealed a positive association between birth weight and cord blood BPA concentration (ß = 0.26; p = 0.02). Further research on maternal exposure during the fetal and neonatal period is critical for public health.

Evaluation of the effects of herpes simplex glycoprotein B on complement system and cytokines in in vitro models of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder that causes memory loss and dementia and is characterized by a decline in cognitive functions. Brain infections, especially induced by herpes simplex virus type-1 (HSV-1), are suggested to play a key role in the pathogenesis of AD. Within the scope of this study, two different AD models (Tau model and amyloid beta [Aß]) were created in the SH-SY5Y cell line, and HSV glycoprotein B (gB) was applied to the cell line and on the generated AD models. Study groups (n = 3) were designed as (1) control, (2) HSV-gB group, (3) retinoic acid (RA) and brain derived neurotrophic factor (BDNF) induced Alzheimer's model (AD), (4) RA and BDNF induced Alzheimer's model + HSV-gB (ADH), (5) Aß 1-42 peptide-induced Alzheimer's model (Aß), and (6) Aß 1-42 peptide-induced Alzheimer's model + HSV-gB (AßH). Levels of complement proteins and cytokines were determined comparatively. In addition, specific markers of AD (hyperphosphorylated Tau proteins, Aß 1-40 peptide and amyloid precursor protein) were measured in all groups. HSV-gB administration was found to increase Aß and hyperphosphorylated Tau levels, similar to AD models. In addition, our data confirmed that the immune system and chronic inflammation might have a crucial role in AD development and that HSV-1 infection might also be an underlying factor of AD.

Estimated exposure to bisphenol A in breastfed and breastfed plus formula-fed infants in Turkey: a comparison study.

This study aimed to estimate and compare dietary exposure to bisphenol A (BPA) in exclusively breastfed (EBF) and breastfed plus formula-fed (BF + FF) infants. A total of 70 mothers and their 0-6 month-old infants (40 in the EBF group and 30 in BF + FF group) were included in the study. After the questionnaire form was applied to the mothers, maternal breast milk, infant formula, and infant urine were collected from mother-infant dyads. Total BPA levels in breast milk, infant formula, and infant urine samples were analyzed by the high-pressure liquid chromatography (HPLC). While BPA was detected in 92.5% of the breast milk samples in the EBF group (mean ± SD = 0.59 ± 0.29 ng/mL), BPA was detected in all of the breast milk samples in the BF + FF group (mean ± SD= 0.72 ± 0.37 ng/mL) (p < 0.05). Similarly, 100% of the infant formula samples in the BF + FF group had detectable levels of BPA (mean ± SD = 7.54 ± 1.77 ng/g formula). The mean urinary BPA levels in the EBF infants (4.33 ± 1.89 µg/g creatinine) were not statistically different from the BF + FF infants (5.81 ± 0.11 µg/g creatinine) (p > 0.05). The average daily BPA intake in EBF infants (0.18 ± 0.13 µg/kg body weight (bw)/day) was found to be significantly higher than in BF + FF infants (0.12 ± 0.09 µg/kg bw/day) (p < 0.05). The estimated dietary intakes of BPA for infants in both groups were below the temporary tolerable daily intake (t-TDI) (4 µg/kg bw/day). Consequently, BPA intake of EBF and BF + FF infants were within safe daily limits during the first six months of life.

Evaluation of the toxic effects of thimerosal and/or aluminum hydroxide in SH-SY5Y cell line.

In this study, we aimed to evaluate possible toxic effects of thimerosal, aluminum and combination of thimerosal and aluminum in SH-SY5Y cells. Inhibitory concentrations were determined by MTT assay; reactive oxygen species (ROS) were determined by a fluorometric kit and antioxidant/oxidant parameters were measured by spectrophotometric kits. Nuclear factor erythroid 2-associated factor 2 (Nrf2), norepinephrine (NE), dopamine transporter (DAT) and dopamine beta ß-hydroxylase (DBH) levels were measured by sandwich ELISA kits while 8-hydroxy deoxyguanosine (8-OHdG) and dopamine levels were determined by competitive ELISA kits. Thimerosal (1.15 µM) and aluminum (362 µM) were applied to cells at inhibitory concentrations 20 (IC20s) for 24 h. ROS increased significantly in cells aluminum- and aluminum+thimerosal-treated cells. Glutathione levels decreased in aluminum group while total antioxidant capacity and protein oxidation levels increased significantly in aluminum and aluminum+thimerosal groups. Lipid peroxidation increased significantly in groups treated with aluminum and aluminum+thimerosal. Nrf2 levels and DNA damage were significantly higher in all groups while dopamine levels significantly increased in cells treated with thimerosal and aluminum+thimerosal, DAT levels were found to be higher in all experimental groups compared to the control. These findings showed that both thimerosal and aluminum can change oxidant/antioxidant status, cause DNA damage, alter dopamine and DAT levels. Changes seen in cells treated with combined exposure to aluminum and thimerosal are more pronounced. Special care should be taken while vaccinating sensitive populations and safer alternatives for aluminum and thimerosal should used.

Modification of the toxic effects of methylmercury and thimerosal by testosterone and estradiol in SH-SY5Y neuroblastoma cell line.

Short-chained alkyl mercury compounds accumulate in particularly in the brain. Exposure to these compounds is associated with various neurotoxic effects. Gender-based differences are observed in neurodevelopmental disorders, and testosterone and estradiol may alter the toxic effect of the compounds. The present study aimed to investigate the toxic effects of methylmercury and thimerosal on SH-SY5Y cells in high testosterone/low estradiol and high estradiol/low testosterone containing cellular environment and estimate whether male and female brains react differently to the toxic effects of methylmercury and thimerosal. Study groups (n = 3) were designed as control: growth medium, thimerosal (T): 1.15-µM thimerosal, methylmercury (M): 2.93-µM methylmercury, high testosterone/low estradiol + thimerosal (TT): 1-µM testosterone + 0.75-µM estradiol + 1.15-µM thimerosal, high estradiol/low testosterone + thimerosal (ET): 0.1-µM testosterone + 7.5-µM estradiol + 1.15-µM thimerosal, high testosterone/low estradiol + methylmercury (TM): 1-µM testosterone + 0.75-µM estradiol + 2.93-µM methylmercury and high estradiol/low testosterone + methylmercury (EM): 0.1-µM testosterone + 7.5-µM estradiol + 2.93-µM methylmercury. While a significant decrease in glutathione levels was observed in M group, it was not seen in EM group. A significant increase in the protein carbonyl levels was detected in T group. A similar increase was observed in the TM and TT groups in which testosterone was dominant. It was determined that methylmercury, but not thimerosal, caused significant DNA damage and in TT group. The results showed that both thimerosal and methylmercury are toxic on SH-SY5Y cells and toxic effects of methylmercury are more severe than thimerosal. It has been determined that testosterone and estradiol alter the toxic effects of thimerosal and methylmercury.