Toxic effects of Aroclor 1254 on rat liver and modifying roles of selenium.

Polychlorinated biphenyls (PCBs) were used in different industrial areas and banned due to their high toxicity. Aroclor 1254 (A1254), commercial PCB congener, accumulates in environment leading to high human exposure. A1254 may cause hepatotoxicity, metabolic and endocrine disorders. In our study, 3-week-old male rats were separated into 6 groups: C (0.15 mg/kg Se in diet); SeS (1 mg/kg Se in diet); SeD (0.05 mg/kg Se in diet); A1254 receiving groups (A; ASeS; ASeD) were given 10 mg/kg/day A1254 orally for last 15 days of feeding period with control, SeD or SeS diet, respectively, for 5 weeks. Histopathology, oxidant/antioxidant balance, apoptosis and cell cycle proteins (p53, p21) in liver were evaluated. Our results suggest that A1254 leads to changes in histology, oxidative stress and apoptosis. Selenium deficiency augments oxidative stress and apoptosis while selenium supplementation is partially protective. More mechanistic in vivo experiments are necessary for evaluation of hepatotoxicity of PCBs.

Comparative evaluation of the effects of bisphenol derivatives on oxidative stress parameters in HepG2 cells.

Bisphenol A (BPA) BPA is an endocrine-disrupting chemical that has a wide range of uses. Exposure to BPA can be by oral, inhalation, and parenteral routes. Although its use in several products is limited, there is still concern on its adverse health effects, particularly for susceptible populations like children. Alternative bisphenols, such as bisphenol S (BPS) and bisphenol F (BPF), are now being used instead of BPA, although there is little information on the toxicity of these bisphenols. BPF is used as a plasticizer in the production of several industrial materials as well as in the coating of drinks and food cans. BPS is used in curing fast-drying epoxy glues, as a corrosion inhibitor and as a reactant in polymer reactions. In this study, the possible toxic effects of BPA, BPS, and BPF in HepG2 cells were evaluated comparatively. For this purpose, their effects on cytotoxicity, production of intracellular reactive oxygen species (ROS), oxidant/antioxidant parameters, and DNA damage have been examined. The cytotoxicity potentials of different bisphenols were found to be as BPS > BPF > BPA. All bisphenol derivatives caused increases in intracellular ROS production. We observed that all bisphenol derivatives cause an imbalance in some oxidant/antioxidant parameters. Bisphenols also caused significant DNA damage in order of BPF > BPA > BPS. We can suggest that both of the bisphenol derivatives used as alternatives to BPA also showed similar toxicities and may not be considered as safe alternatives. Mechanistic studies are needed to elucidate this issue.

Effects of single or combined exposure to bisphenol A and mono(2-ethylhexyl)phthalate on oxidant/antioxidant status, endoplasmic reticulum stress, and apoptosis in HepG2 cell line.

Endocrine disrupting chemicals (EDCs) may affect many biological processes like growth and stress response. Bisphenol A (BPA) is a plasticizer that is used to harden plastics and polycarbonates. Phthalates are used to add flexibility to polyvinyl chloride containing plastics. The main metabolite of di(2-ethylhexyl) phthalate (DEHP) is mono(2-ethylhexyl) phthalate (MEHP) and it is even more toxic than the parent compound. Humans are usually exposed to these chemicals in mixtures by different routes starting from fetal period. However, there are not many studies in literature that investigate the combined effects of these chemicals. The aim of this study is to investigate toxic effects of BPA and/or MEHP on HepG2 cell line. We have evaluated cytotoxicity, cytomorphological, apoptotic changes, oxidative stress, oxidant/antioxidant status alterations, and endoplasmic reticulum (ER) stress. Combined exposure to BPA and MEHP caused alterations in oxidant/antioxidant status and ER stress marker proteins in both cytoplasmic and nuclear cellular fractions. We can suggest that combined exposure to EDCs may cause serious toxicological outcomes and more mechanistic studies are needed to determine the combined toxic effects.

The effects of prenatal and lactational bisphenol A and/or di(2-ethylhexyl) phthalate exposure on female reproductive system.

Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine disrupting chemicals (EDCs) that are abundantly used in polyvinyl chloride plastics, polycarbonates and epoxy resins. Prenatal and early postnatal exposures to EDCs are suggested to be more critical. Such exposures can lead to reprotoxic effects, hormonal and metabolic consequences in adulthood. Moreover, combined exposure to different EDCs can lead to more serious adverse effects, some of which cannot be predicted by examining their individual toxicity profiles. This study aimed to evaluate effects of single and combined prenatal and lactational exposures to BPA and/or DEHP on female reproductive hormones and ovarian follicle development. Pregnant Sprague-Dawley rats were divided randomly to four groups (n = 3/group): Control (received vehicle only); DEHP (30 mg/kg/day); BPA (50 mg/kg/day) and BPA + DEHP (30 mg/kg/day DEHP; 50 mg/kg/day BPA) through 6-21 gestational days and lactation by intra-gastric lavage. Female offspring (n = 6/group) were fed until the end of twelfth postnatal week and then euthanized. Reproductive hormones, ovarian follicle numbers and ovarian development were determined. Plasma testosterone and estradiol levels of BPA and BPA + DEHP groups were significantly lower than control. In BPA group, the number of tertiary ovarian follicles decreased significantly compared to control. In the combined exposure group, the number of corpus luteum (29%), as well as the number of primordial follicles (36%), showed marked decreases compared to control group. It can be suggested that early life exposure to BPA and DEHP may cause late life adverse effects in female reproductive system, especially after combined exposure.

Effects of prenatal and lactational bisphenol a and/or di(2-ethylhexyl) phthalate exposure on male reproductive system.

Bisphenol A (BPA) and phthalates are abundantly used endocrine disrupting chemicals (EDCs). The aim of this study was to evaluate the effects of single and combined exposures to BPA and/or di(2-ethylhexyl) phthalate (DEHP) in prenatal and lactational period on rat male reproductive system in later stages of life. Pregnant Sprague-Dawley rats were divided randomly to four groups (n = 3/group): Control (corn oil); DEHP (30 mg/kg/day); BPA (50 mg/kg/day); and BPA+ DEHP (30 mg/kg/day DEHP and 50 mg/kg/day BPA). Groups exposed to EDCs through 6-21 gestational days and lactation period by intragastric lavage. Male offspring (n = 6/group) from each mother were fed till adulthood and were then euthanized. Later, reproductive hormones, sperm parameters, and oxidative stress parameters were determined. In conclusion, we can suggest that prenatal and lactational exposure to BPA and DEHP may cause adverse effects in male reproductive system in later stages of life especially after combined exposure.

Neuroendocrine disruption by bisphenol A and/or di(2-ethylhexyl) phthalate after prenatal, early postnatal and lactational exposure.

Bisphenol A (BPA) and di(2-ethylhexyl)phthalate (DEHP) are abundant endocrine disrupting chemicals (EDCs). In recent years, studies showed that EDCs may lead to neurodevelopmental diseases. The effects of prenatal exposure to these chemicals may have serious consequences. Moreover, exposure to EDCs as a mixture may have different effects than individual exposures. The present study aimed to determine the toxicity of BPA and/or DEHP on central nervous system (CNS) and neuroendocrine system in prenatal and lactational period in Sprague-Dawley rats. Pregnant rats were randomly divided into four groups: control (received vehicle); BPA group (received BPA at 50 mg/kg/day); DEHP group (received DEHP at 30 mg/kg/day); and combined exposure group (received both BPA at 50 mg/kg/day and DEHP at 30 mg/kg/day) during pregnancy and lactation by oral gavage. At the end of lactation, male offspring (n = 6) were randomly grouped. The alterations in the brain histopathology, neurotransmitter levels and enzyme activities in the cerebrum region, oxidative stress markers, and apoptotic effects in the hippocampus region were determined at adulthood. The results showed that exposure to EDCs at early stages of life caused significant changes in lipid peroxidation, total GSH and neurotransmitter levels, and activities of neurotransmitter-related enzymes. Moreover, BPA and/or DEHP led to apoptosis and histopathologic alterations in the hippocampus. Therefore, we can suggest that changes in oxidant/antioxidant status, as well as in neurotransmitters and related enzymes, can be considered as the underlying neurotoxicity mechanisms of BPA and DEHP. However, more mechanistic studies are needed.

The association between urinary BPA levels and medical equipment among pediatric intensive care patients.

We aim to evaluate urinary total BPA (tBPA) levels and association with medical devices used on patients in pediatric intensive care units. This cross-sectional descriptive study included 117 critically ill children. Urinary tBPA levels were determined using high-performance liquid chromatography. General estimating equations with repeated measures analyzed the effect of interventions and devices on urinary BPA levels. A total of 292 urine samples taken from 117 child intensive care patients were studied. When age, sex, and body mass index-for age z-scores were controlled, cases having endotracheal intubation showed higher urinary tBPA levels (p = 0.003) and hemodialyzed patients had considerably higher urinary tBPA levels (p = 0.004). When confounding factors were controlled, cases using both multiple iv treatment and more than four medical devices showed higher urinary tBPA levels than their counterparts (p = 0.007 and p = 0.028, respectively). The use of certain medical devices and interventions could increase BPA exposure in pediatric intensive care patients.

Renal changes and apoptosis caused by subacute exposure to Aroclor 1254 in selenium-deficient and selenium-supplemented rats.

Aroclor 1254 (A1254), a mixture of polychlorinated biphenyls, exerts hepatic, renal, and reproductive toxicity in rodents. This study aimed to determine a protective role of selenium on histopathological changes, oxidative stress, and apoptosis caused by A1254 in rat kidney. It included a control group, which received regular diet containing 0.15 mg/kg Se (C), a Se-supplemented group (SeS) receiving 1 mg/kg Se, a Se-deficient group (SeD) receiving Se-deficient diet of ≤0.05 mg/kg Se, an A1254-treated group (A) receiving 10 mg/kg of Aroclor 1254 and regular diet, an A1254-treated group receiving Se-supplementation (ASeS), and an A1254-treated group receiving Se-deficient diet (ASeD). Treatments lasted 15 days. After 24 h of the last dose of A1254, the animals were decapitated under anaesthesia and their renal antioxidant enzyme activities, lipid peroxidation (LP), glutathione, protein oxidation, and total antioxidant capacity levels measured. Histopathological changes were evaluated by light and electron microscopy. Apoptosis was detected with the TUNEL assay. Kidney weights, CAT activities, and GSH levels decreased significantly in all A1254-treated groups. Renal atrophic changes and higher apoptotic cell counts were observed in the A and ASeD groups. Both groups also showed a significant drop in GPx1 activities (A - 34.92 % and ASeD - 86.46 %) and rise in LP (A - 30.45 % and ASeD - 20.44 %) vs control. In contrast, LP levels and apoptotic cell counts were significantly lower in the ASeS group vs the A group. Histopathological changes and renal apoptosis were particularly visible in the ASeD group. Our findings suggest that selenium supplementation provides partial protection against renal toxicity of Aroclor 1254.

The Effects of Polymer Coating of Gold Nanoparticles on Oxidative Stress and DNA Damage.

Gold nanoparticles (AuNPs) have been widely used in many biological and biomedical applications. In this regard, their surface modification is of paramount importance in order to increase their cellular uptake, delivery capability, and optimize their distribution inside the body. The aim of this study was to examine the effects of AuNPs on cytotoxicity, oxidant/antioxidant parameters, and DNA damage in HepG2 cells and investigate the potential toxic effects of different surface modifications such as polyethylene glycol (PEG) and polyethyleneimine (PEI; molecular weights of 2,000 (low molecular weight [LMW]) and 25,000 (high molecular weight [HMW]). The study groups were determined as AuNPs, PEG-coated AuNPs (AuNPs/PEG), low-molecular weight polyethyleneimine-coated gold nanoparticles (AuNPs/PEI LMW), and high-molecular weight polyethyleneimine-coated gold nanoparticles (AuNPs/PEI HMW). After incubating HepG2 cells with different concentrations of nanoparticles for 24 hours, half maximal inhibitory concentrations (the concentration that kills 50% of the cells) were determined as 166.77, 257.73, and 198.44 µg/mL for AuNPs, AuNPs/PEG, and AuNPs/PEI LMW groups, respectively. Later, inhibitory concentration 30 (IC30, the concentration that kills 30% of the cells) doses were calculated, and further experiments were performed on cells that were exposed to IC30 doses. Although intracellular reactive oxygen species levels significantly increased in all nanoparticles, AuNPs as well as AuNPs/PEG did not cause any changes in oxidant/antioxidant parameters. However, AuNPs/PEI HMW particularly induced oxidative stress as evidence of alterations in lipid peroxidation and protein oxidation. These results suggest that at IC30 doses, AuNPs do not affect oxidative stress and DNA damage significantly. Polyethylene glycol coating does not have an impact on toxicity, however PEI coating (particularly HMW) can induce oxidative stress.

Histopathologic, apoptotic and autophagic, effects of prenatal bisphenol A and/or di(2-ethylhexyl) phthalate exposure on prepubertal rat testis.

Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine-disrupting chemicals (EDCs) used in a wide variety of industrial products as plasticizers. Exposure to EDCs, particularly in mixtures, in prenatal and early postnatal periods may lead to unwanted effects and can cause both developmental and reproductive problems. In this study, we aimed to determine the individual and combined effects of prenatal and lactational exposure to BPA and/or DEHP on testicular histology, apoptosis, and autophagic proteins. Pregnant Sprague-Dawley rats (n = 3) were divided into four groups (control, BPA (50 mg/kg/day), DEHP (30 mg/kg/day), and BPA (50 mg/kg/day) + DEHP (30 mg/kg/day)) and dosed by oral gavage during pregnancy and lactation. The male offspring (n = 6) from each group were chosen randomly, and their testicular examinations were performed on the twelfth week. The results showed that fetal and neonatal exposure to BPA and DEHP could lead to significant testicular histopathological alterations and cause increases in apoptosis markers (as evidenced by increases in caspase 3 and caspase 8 levels; increased TUNEL-positive spermatogonia and TUNEL-positive testicular apoptotic cells) and autophagic proteins (as evidenced by increased LC3 and Beclin levels and decreased p62 levels) in testicular tissue. We can suggest that EDCs cause more dramatic changes in both testicular structure and cell death when there is combined exposure.

The effects of different bisphenol derivatives on oxidative stress, DNA damage and DNA repair in RWPE-1 cells: A comparative study.

Bisphenol A (BPA) is a well-known endocrine disruptor and it is widely used mainly in the plastics industry. Due to recent reports on its possible impact on health (particularly on the male reproductive system), bisphenol F (BPF) and bisphenol S (BPS) are now being used as alternatives. In this study, RWPE-1 cells were used as a model to compare cytotoxicity, oxidative stress-causing potential and genotoxicity of these chemicals. In addition, the effects of the bisphenol derivatives were assessed on DNA repair proteins. RWPE-1 cells were incubated with BPA, BPF, and BPS at concentrations of 0-600 µM for 24 h. The inhibitory concentration 20 (IC20 , concentration that causes 20% of cell viability loss) values for BPA, BPF, and BPS were 45, 65, and 108 µM, respectively. These results indicated that cytotoxicity potentials were ranked as BPA > BPF > BPS. We also found alterations in superoxide dismutase, glutathione peroxidase and glutathione reductase activities, and glutathione and total antioxidant capacity in all bisphenol-exposed groups. In the standard and modified Comet assay, BPS produced significantly higher levels of DNA damage vs the control. DNA repair proteins (OGG1, Ape-1, and MyH) involved in the base excision repair pathway, as well as p53 protein levels were down-regulated in all of the bisphenol-exposed groups. We found that the BPA alternatives were also cytotoxic and genotoxic, and changed the expressions of DNA repair enzymes. Therefore, further studies are needed to assess whether they can be used safely as alternatives to BPA or not.

Oxidative Stress Parameters, Selenium Levels, DNA Damage, and Phthalate Levels in Plastic Workers.

Di(2-ethylhexyl)phthalate (DEHP) is the most widely used phthalate. DEHP is highly used in PVC floorings and PVC windows and carpeting. The objective of this study was to determine sex hormone levels, oxidative stress parameters, selenium levels, DNA damage, and phthalate levels in plastics workers (n = 24, age = 20-58 years) working in the production of rubber mechanical goods and exposed to DEHP in workplace. The control group (n = 29, age = 25-54, all male) was selected from age-matched healthy adults. Antioxidant parameters and DNA damage were determined by spectrophotometry. Selenium levels were determined by atomic absorption spectroscopy. Plasma hormone levels were measured by chemiluminescence microparticle immunoassay. Plasma phthalate levels were determined by high-pressure liquid chromatography. Plastic workers had lower serum testosterone and free T4 levels and higher follicle-stimulating hormone levels vs. controls. Liver enzyme activities were markedly higher in workers vs. controls. There were also increases in plasma glutathione peroxidase levels and marked decreases in plasma selenium and erythrocyte total glutathione levels in plastics workers (P < 0.05 vs. control). Plasma 8-hydroxy-2'-deoxyguanosine levels were 14-fold higher in plastics workers than in controls. Plasma DEHP and mono(2-ethylhexyl)phthalate were also markedly higher in workers vs. controls. The results of this study show that occupational exposure to DEHP may lead to disturbances in sex hormones, increased liver problems, higher oxidative stress and DNA damage levels, and lower trace element concentrations in workers. More comprehensive and mechanistic studies with higher numbers of subjects are needed to show the unwanted effects of occupational exposure to DEHP.

Oxidative stress markers, trace elements, and endocrine disrupting chemicals in children with Hashimoto's thyroiditis.

In this study, we aimed to investigate whether bisphenol A (BPA) and di-(2-ethylhexyl) phthalate (DEHP) exposure have any association with Hashimoto's thyroiditis (HT) and its biomarkers and to determine whether oxidative stress biomarkers and trace element levels showed any alterations in children with HT. We found that superoxide dismutase and glutathione peroxidase activities are lower in HT group from control (24% and 46%, respectively, p < 0.05). Zinc levels were significantly lower in HT group vs. control. In addition, the levels of mono-(2-ethylhexyl) phthalate (MEHP) which is the primary metabolite for DEHP, were markedly higher in HT group compared to control (p < 0.05). A negative correlation was observed between urinary BPA levels and fT4. In children with HT, oxidant/antioxidant balance is changed and these differences may be related by EDC exposure, the importance of which should be elucidated with further studies.

Bisphenol A and phthalate levels in adolescents with polycystic ovary syndrome.

Endocrine disruptors have been proposed in the etiology of polycystic ovary syndrome (PCOS) as they have the potency to interfere with hormone-sensitivity systems. The aim of this study was to evaluate the levels of bisphenol A (BPA) and phtalates in adolescents with PCOS. Sixty-two girls with PCOS and 33 controls, age 12-18 years were enrolled in the study. The diagnosis of PCOS was made using modified Rotterdam criteria. Urinary BPA levels were measured using high-performance liquid chromatography. Di-(2-ethylhexyl)-phthalate (DEHP), the most commonly used phthalate and mono-(2-ethylhexyl)-phthalate (MEHP), its main metabolite were measured by using high-performance liquid chromatography. Adolescents with PCOS had markedly increased BPA levels (15.89 µg/g creatine ± 1.16) when compared with the control group (7.30 µg/g creatine ± 1.38) (p = .016). In adolescents with PCOS, BPA was significantly correlated with polycystic morphology on ultrasound but not with obesity androgen levels, or other metabolic parameters. Patients with PCOS (DEHP: 0.40 ppm ± 0.24, MEHP: 0.13 ppm ± 0.23) and controls (DEHP: 0.49 ppm ± 0.27, MEHP: 0.14 ppm ± 0.3) had similar serum phtalate concentrations (p = .7 and p = .3, respectively). Exposure to specific endocrine disruptors such as BPA could modify neuroendocrine, reproductive, and metabolic regulation favoring PCOS development in adolescents.

The effects of amniotic fluid and foetal cord blood cotinine concentrations on pregnancy complications and the anthropometric measurements of newborns.

Our objective was determining the effects of amniotic fluid (AF) and fetal cord blood (FCB) cotinine concentrations on pregnancy complications and the anthropometric measurements in the newborns whose mothers underwent amniocentesis. This study was conducted as a case-control study, in Turkey. A total of 250 pregnant women with amniocentesis indication were recruited into the study and the cotinine levels in the AF and FCB were determined. A smoking habit did not statistically affect the incidence of pregnancy complications (p>.05). The birth weights of the newborns were negatively correlated with the AF cotinine levels. The incidences of low birth weight, low Apgar scores and RDS were positively correlated with higher levels of cotinine in AF and FCB. It is important for healthcare staff to provide training and consultancy services for the health improvement of pregnant women and the prevention of smoking during pregnancy. Impact statement What is already known on this subject? The pre-pregnancy smoking habit usually continues during the pregnancy. A significant negative correlation was present between the foetal cord blood cotinine levels and the birth weight. What do the results of this study add? The anthropometric measurements of the newborns born from mothers with high AF cotinine levels were lower than newborns born from mothers with low amniotic fluid cotinine levels. Respiratory Distress syndrome is more often determined in newborns born from mothers with high AF cotinine levels. What are the implications of these findings for clinical practice and/or further research? Future studies should be performed to investigate the effects of cigarette smoking on the health problems, the growth characteristics and the neurological development of newborns and infants within the first year of life.

Prenatal bisphenol a and phthalate exposure are risk factors for male reproductive system development and cord blood sex hormone levels.

Bisphenol A (BPA) and phthalates can adversely affect the fetal development. However, observational studies on the effects of these chemicals on fetal male reproductive system are still limited. A hundred of umbilical cord blood samples were analyzed for the levels of BPA, di-2-ethylhexyl phthalate (DEHP), mono-2-ethylhexyl phthalate (MEHP), and sex hormones. After birth, male newborns underwent physical examination that included measurements of anogenital distance, stretched penile length (SPL), and penile width. BPA, DEHP and MEHP levels were detectable in ≈99% of cord blood samples. In covariate-adjusted models, cord blood BPA levels were inversely associated with SPL of newborns and positively associated with cord blood estradiol levels. In addition, there was a significant inverse relationship between cord blood DEHP levels and anogenital distance index of newborn males. Our results suggest that in utero BPA and DEHP exposure exerted adverse effects on fetal male reproductive development and cord blood estradiol levels.

Antioxidants and selenocompounds inhibit 3,5-dimethylaminophenol toxicity to human urothelial cells.

Exposure to alkyl anilines may lead to bladder cancer, which is the second most frequent cancer of the urogenital tract. 3,5-dimethylaniline is highly used in industry. Studies on its primary metabolite 3,5-dimethylaminophenol (3,5-DMAP) showed that this compound causes oxidative stress, changes antioxidant enzyme activities, and leads to death of different mammalian cells. However, there is no in vitro study to show the direct effects of 3,5-DMAP on human bladder and urothelial cells. Selenocompounds are suggested to decrease oxidative stress caused by some chemicals, and selenium supplementation was shown to reduce the risk of bladder cancer. The main aim of this study was to investigate whether selenocompounds organic selenomethionine (SM, 10 µmol/L) or inorganic sodium selenite (SS, 30 nmol/L) could reduce oxidative stress, DNA damage, and apoptosis in UROtsa cells exposed to 3,5-DMAP. 3,5-DMAP caused a dose-dependent increase in intracellular generation of reactive oxygen species, and its dose of 50 µmol/L caused lipid peroxidation, protein oxidation, and changes in antioxidant enzyme activities in different cellular fractions. The comet assay also showed single-strand DNA breaks induced by the 3,5-DMAP dose of 50 µmol/L, but no changes in double-strand DNA breaks. Apoptosis was also triggered. Both selenocompounds provided partial protection against the cellular toxicity of 3,5-DMAP. Low selenium status along with exposure to alkyl anilines can be a major factor in the development of bladder cancer. More mechanistic studies are needed to specify the role of selenium in bladder cancer.

Lead and Mercury Levels in Preterm Infants Before and After Blood Transfusions.

Very low birth weight (VLBW) infants usually receive packed red blood cell unit (pRBC) transfusions. Heavy metal transfer via pRBCs is not widely discussed before. This study aimed to determine pre-/post-transfusion erythrocyte lead and mercury levels in infants and to correlate these levels to heavy metal concentrations in pRBCs. VLBW infants (n = 80), needing pRBC transfusion for the first time, were enrolled. Erythrocyte heavy metal levels were determined in pre-/post-transfusion blood samples and also in pRBC units. Mean lead and mercury levels in the pRBCs were found to be 16.3 ± 10.8 and 3.75 ± 3.23 µg/L, respectively. Of the infants, 69.7% received lead above reference dose. Erythrocyte lead levels increased significantly after transfusions (10.6 ± 10.3 vs. 13 ± 8.5, p < 0.05) with significant correlated to amount of lead within pRBCs (r = 0.28). Mean pre-/post-transfusion erythrocyte mercury levels were 3.28 ± 3.08 and 3.5 ± 2.83 µg/L, respectively (p > 0.05). There was a significant correlation between mean difference of mercury levels after transfusion and amount of mercury delivered by pRBCs (r = 0.28). Infants can be subject to high levels of lead and mercury through pRBC transfusions.

Evaluation of skin irritation potentials of different cosmetic products in Turkish market by reconstructed human epidermis model.

Human skin is a protective barrier against the toxic effects of cosmetics. Marketing of cosmetic products with ingredients tested on animals was prohibited in 2013. Since then, safety evaluation of cosmetic products is performed by using alternative in vitro toxicity tests. In vitro 3-D reconstructed human epidermis (RhE) tissue models are now used to define skin irritation/corrosion potentials of cosmetic ingredients and end-products. The main aim of this study was to evaluate skin irritation potentials of topically used cosmetic end-products which were marketed in Turkey during 2015-2017, by using the EpiDerm in vitro 3D-human skin model. Sixty widely used cosmetic products were collected from different markets/cosmetic shops. Among hair care products, only one shampoo was found to be strong/severe skin irritant/possible corrosive while 22 shampoos were moderate skin irritant and 11 shampoos were moderate to mild skin irritant. Among 6 skin care products, one was found to be moderate to mild skin irritant. We can suggest that alternative in vitro tests should continuously be used to test both the ingredients and the final cosmetic formulations.

Assessment of oxidant-antioxidant status alterations with tumor biomarkers and reproductive system hormones in uterine MYOMAS.

OBJECTIVES: Uterine myomas (UM) are responsible for significant morbidity and have adverse effects on quality of life in women. Reactive oxygen species (ROS) and antioxidant enzymes (AOE), as well as sex steroids play important roles in the reproductive physiology processes. Thus, we aimed to investigate the role of oxidant-antioxidant status in UM by measuring the AOE activities and lipid peroxidation (LPO) levels. This is the first study assessing these parameters together in UM based on also menopausal status and evaluating possible correlations between AOE activities, LPO markers, tumor biomarkers, female reproductive system hormone levels, comprehensively. STUDY DESIGN: The study group consisted of patients who have undergone surgical resection with confirmed pathology of uterine myoma (UM, n = 25) and divided into subgroups; premenopausal (UMpre) and postmenopausal (UMpost). Erythrocyte copper-zinc superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GPx1) activities were measured along with plasma malondialdehyde (MDA) and urinary 8-epi-prostaglandin F2α (8-epi-PGF2α) levels in patients with UM. The obtained data were compared to the data of healthy individuals (C, n = 25) and its subgroups; premenopausal (Cpre) and postmenopausal (Cpost). RESULTS: All AOE activities were higher (∼40% for Cu,Zn-SOD, p = 0.003; ∼55% for CAT, p = 0.001; ∼15% for GPx1, p = 0.169) and the LPO levels were lower (∼60% for MDA, p = 0.011 and ∼45% for 8-epi-PGF2α, p = 0.055) in patients with UM vs control. Approximately similar alterations were observed in UMpre vs Cpre and in UMpost vs Cpost. A significant negative correlation between erythrocyte Cu,Zn-SOD activity and plasma MDA levels (r = -0.431, p = 0.005) was reported. CONCLUSION: Decreased LPO levels might be the consequence of compensator high antioxidant enzyme activities against mild oxidative stress in the circulation of patients with UM. The marked negative correlation between erythrocyte Cu,Zn-SOD activity and plasma MDA levels also supported this finding.