Exposure to endocrine disrupting chemicals (EDCs), particularly during developmental periods, gives rise to a variety of adverse health outcomes. Bisphenol A (BPA) is a well-known EDC commonly found in plastic products including food and water containers, baby bottles, and metal can linings. This study investigates infant exposure to BPA and the effect of bottle-feeding on serum BPA levels in infants. Serum BPA levels in normal healthy infants 6 to 15 months of age (n=60) were evaluated by a competitive ELISA. BPA was detected in every study sample. Serum BPA levels of bottle-fed infants (n=30) were significantly higher than those of breast-fed infants (n=30) (96.58+/-102.36 vs 45.53+/-34.05 pg/mL, P=0.014). There were no significant differences in serum BPA levels between boys (n=31) and girls (n=29). No significant correlations were found between serum BPA levels and age, body weight, birth weight, and gestational age. Bottle-feeding seems to increase the risk of infant exposure to BPA. Establishment of health policies to reduce or prevent BPA exposure in infants is necessary.
Benzhydryl Compounds/*blood ; Birth Weight ; Body Weight ; Bottle Feeding ; Endocrine Disruptors/*blood ; Environmental Exposure ; Female ; Humans ; Infant ; Male ; Phenols/*blood

OBJECTIVETo monitor the biological levels of environmental endocrine disruptors (EDs, phthalates and surfactants) in the umbilical cord blood and maternal blood of low-birth-weight infants.

METHODSAll 30 umbilical cord blood samples and 21 maternal blood samples were collected from low-birth-weight infants. The concentration of four kinds of phthalates (di-2-ethylhexyl phthalate, DEHP; mono-2-ethylhexyl phthalate, MEHP; di-ethyl phthalate, DEP; di-n-butyl phthalate, DBP) and two kinds of surfactants (4-nonylphenol, 4-NP; octylphenol, OP) in these blood samples were measured by using reversed-phase high performance liquid chromatography.

RESULTSThe mean birth weight and birth length of low-birth-weight infants were (2158.48 +/- 125.06) g and (45.36 +/- 2.52) cm, respectively. The concentrations of DEP, MEHP, DBP, DEHP, 4-NP and OP were 18.90, 11.87, 7.67, 8.84, 1.51 and 2. 86 mg/L in maternal blood, and the detective rates were 86.7%, 63.3%, 60.0%, 63.3%, 56.7% and 66.7%, respectively. In umbilical cord blood, the concentrations of those EDs were 11.92, 9.94, 5.71, 5.20, 1.12 and 1.19 mg/L; the detective rates were 86.7%, 63.3%, 60.0%, 63.3%, 56.7% and 66.7%. No matter in maternal blood or in umbilical cord blood, the contents and detective rates of phthalates were higher than the surfactants. The concentration of MEHP was higher than its primer, DEHP. The contents of the target EDs in umbilical cord blood were less than those in the matched maternal blood. The percentages were 47.82% -84.05%.

CONCLUSIONPeople could be exposed to EDs from embryo period. And this should be paid attention by the related departments.

Diethylhexyl Phthalate ; blood ; Endocrine Disruptors ; blood ; Fetal Blood ; chemistry ; Humans ; Infant ; Infant, Low Birth Weight ; blood ; Infant, Newborn ; Mothers ; Surface-Active Agents

OBJECTIVETo investigate the role of environmental endocrine disruptors (EEDs) in causing the precocious puberty.

METHODSThe blood samples were collected from 79 cases of precocious puberty patients and 42 cases of normal children. The concentrations of 4-nonylphenol (4-NP), 1, 1-dichloro-2, 2, bis (p-chlorophenyl) ethylene (p, p'-DDE) and di-2-ethylhexyl phthalate (DEHP) in blood serum samples were measured by using reversed-phase high performance liquid chromatography (HPLC). The volume of uterus and ovary, the bone density, and the content of estradiol (E(2)) in serum were determined at the same time. The contents of EEDs in blood serums of precocious puberty and the indices of the target organs were analyzed by using of correlation and regression.

RESULTSIn normal control group, p, p'-DDE was detected in all the blood samples (14.93 - 40.39 ng/ml), but 4-NP and DEHP were detected in some samples (ND -6.77 ng/ml, ND -17.61 ng/ml). The levels of 4-NP, p, p'-DDE and DEHP in blood serum in precocious puberty group were notably increased than that in control group (P < 0.01). In precocious puberty group, there was a positive correlations between the 4-NP in volume of uterus and the volume of ovary and the density of bone (r = 0.394, 0.286, 0.237, P < 0.01); p, p'-DDE and volume of uterus also showed a the positive correlation (r = 0.306, P < 0.01). The influencing extent of 4-NP was 1.3 times to that of the p, p'-DDE.

CONCLUSIONThe normal children and the children with precocious puberty should be all contaminated by EEDs, and the later be exposured to more EEDs. There might exist a close relationship between EEDs and the precocious puberty, and EEDs should be an important factor in causing the disease. Different kinds of EEDs might have different influencing extents to the target organs.

Case-Control Studies ; Child ; Child, Preschool ; Chromatography, High Pressure Liquid ; Dichlorodiphenyl Dichloroethylene ; blood ; Endocrine Disruptors ; blood ; Female ; Humans ; Male ; Polychlorinated Biphenyls ; blood ; Puberty, Precocious ; blood

OBJECTIVETo verify the antagonistic effect of Bushen Tianjing Recipe (BTR) on environmental endocrine disruptors (EEDs) induced gonadal dysgenesis (GD) Sprague-Dawley (SD) male rat model.

METHODSTotally 70 3-week-old male SD rats were randomly divided into seven groups, i.e., the control group (fed with corn oil), the model A group [di-2-ethylhexyl-phthalate (DEHP) 500 mg/kg], the CM A group (fed with DEHP 500 mg/kg + BTR 40 mL/kg), the exposed group B (fed with CYP 80 mg/kg), the CM B group (fed with CYP 80 mg/kg + BTR 40 mL/kg), the model C group [fed with DEHP 500 mg/kg + CYP 80 mL/kg], the CM C group (DEHP 500 mg/kg + CYP 80 mg/kg + BTR 40 mL/kg), respectively, 10 in each group. All were administered with corresponding medication by gastrogavage, once daily, for total 30 days. Rats were killed 24 h after the last administration, and their body weight and wet testis weight were weighed. The coefficient of testis was calculated. The serum testosterone (T) level was measured by chemiluminescent immunoassay. The histopathologic tissue was prepared. The ultrastructural changes of genital cells were observed by electron microscope.

RESULTSCompared with the control group, there was no statistical difference in the body weight increase among all groups (P > 0.05). The time of testicular descent and preputial separation were significantly delayed in each exposed group (P < 0.01). In the exposed group A and the exposed group C, the wet weight of the testes was reduced and serum T level decreased (P < 0.01). The coefficient of testis significantly decreased in the exposed group A (P < 0.01). Compared with corresponding model group, the time of testicular descent and preputial separation were significantly fore-laid in each corresponding CM group (P < 0.01). The weight of the testes, the coefficient of testis, and the serum T level increased in the CM A group (P < 0.01). The serum T level obviously increased in the CM B group (P < 0.05).

CONCLUSIONSThe GD rat model was successfully duplicated by using DEHP. EEDs were proved to have significant anti-androgen activities. BTR was verified to have significant antagonistic to its anti-androgen effect.

Animals ; Diethylhexyl Phthalate ; toxicity ; Drugs, Chinese Herbal ; therapeutic use ; Endocrine Disruptors ; toxicity ; Gonadal Dysgenesis ; chemically induced ; drug therapy ; Male ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Testosterone ; blood

OBJECTIVETo investigate the relationship between 8 endocrine-disrupting chemicals in the serum and insulin resistance in patients with polycystic ovary syndrome (PCOS).

METHODSThis study was conducted among 60 patients with PCOS, including 23 with insulin resistance (PCOS-IR) and 37 without insulin resistance (PCOS-NIR), and 29 non-PCOS women seeking medical attention for infertility or menstrual disorder (control group). The serum levels of 6 phthalic acid esters (PEAs), bisphenol A (BPA) and octylphenol (OP) were measured in all the subjects.

RESULTSThe levels of PAEs, BPA and OP showed no significant differences between PCOS patients and the control group (P>0.05). The serum level of OP was significantly lower in patients PCOS-IR than in those with PCOS-NIR (47.89 ng/ml vs 60.24 ng/ml, P<0.05).

CONCLUSIONPEAs and BPA do not produce obvious effect on the pathogenesis of PCOS or contribute to insulin resistance, but OP may play a role in insulin resistance in PCOS patients.

Adult ; Benzhydryl Compounds ; adverse effects ; blood ; Case-Control Studies ; Endocrine Disruptors ; adverse effects ; blood ; Environmental Pollutants ; adverse effects ; blood ; Female ; Humans ; Insulin Resistance ; Phenols ; adverse effects ; blood ; Phthalic Acids ; adverse effects ; blood ; Polycystic Ovary Syndrome ; blood ; physiopathology ; Young Adult

OBJECTIVETo observe the effects of fenvalerate on calcium homeostasis in rat ovary.

METHODSFemale Sprague-Dawley rats were orally given fenvalerate at daily doses of 0.00, 1.91, 9.55, and 31.80 mg/kg for four weeks. The ovary ultrastucture was observed by electron microscopy. Serum free calcium concentration was measured by atomic absorption spectrophotometry. The activities of phosphorylase a in rat ovary were evaluated by the chromatometry. The total content of calmodulin in ovary was estimated by ELISA at each stage of estrous cycle. Radioimmunoassay (RIA) was used to evaluate the level of serum progesterone.

RESULTSHistopathologically, damages of ovarian corpus luteum cells were observed. An increase in serum free calcium concentration was observed in rats treated with 31.80 mg/kg fenvalerate. The activities of phosphorylase a enhanced in all treated groups, and fenvalerate increased the total content of calmodulin significantly in estrus period. Serum progesterone levels declined in fenvalerate exposed rats in diestrus.

CONCLUSIONFenvalerate interferes with calcium homeostasis in rat ovary. Also, the inhibitory effects of fenvalerate on serum progesterone levels may be mediated partly through calcium signals.

Animals ; Calcium ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Calmodulin ; metabolism ; Endocrine Disruptors ; toxicity ; Female ; Homeostasis ; drug effects ; Insecticides ; toxicity ; Nitriles ; toxicity ; Ovary ; drug effects ; metabolism ; pathology ; Progesterone ; blood ; Pyrethrins ; toxicity ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the endocrine disrupting effects of cadmium (Cd) using OECD enhanced TG407 test guideline.

METHODSSprague-Dawley (SD) rats were randomly divided into six groups and accordingly administered with 0, 1, 2.5, 5, 10, 20 mg/kg•BW/day of Cd by gavage for 28 days. Body weight, food consumption, hematology, biochemistry, sex hormone levels, urinary β2-microglobulin, organ weights and histopathology and estrous cycle were detected.

RESULTSCd could significantly decrease animals' body weight (P<0.05). Serum luteinizing hormone (LH) at 10-20 mg/kg•BW groups and testosterone (T) at 2.5 and 10 mg/kg•BW groups decreased significantly (P<0.05). However, no statistically significant change was found in urinary β2-microglobulin among Cd-treatment groups (P>0.05). Endpoints related to female reproduction including uterus weight and histopathological change at 10-20 mg/kg•BW groups showed significant increase (P<0.05). While among male rats in 2.5, 10, 20 mg/kg•BW groups, weight of prostate, thyroids, and seminal vesicle glands significantly decreased (P<0.05). Moreover, no histopathological change was observed in kidney.

CONCLUSIONResults suggested that Cd can cause endocrine disrupting effects in SD rats. Comparing with possible renal toxicity of Cd, its toxicity on endocrine system was more sensitive.

Animals ; Body Weight ; drug effects ; Cadmium ; toxicity ; Eating ; drug effects ; Endocrine Disruptors ; toxicity ; Female ; Hormones ; blood ; Kidney ; drug effects ; Male ; Organisation for Economic Co-Operation and Development ; Random Allocation ; Rats, Sprague-Dawley ; Uterus ; drug effects ; beta 2-Microglobulin ; urine

Animals ; Benzhydryl Compounds ; toxicity ; Biomarkers ; analysis ; blood ; Breast Neoplasms ; chemically induced ; Drug Synergism ; Endocrine Disruptors ; toxicity ; Estrone ; metabolism ; Genistein ; adverse effects ; Hydroxyestrones ; analysis ; Male ; Microsomes, Liver ; drug effects ; metabolism ; Oxidation-Reduction ; Phenols ; toxicity ; Rats, Wistar

OBJECTIVETo evaluate the influence of an extract of Genista tinctoria L. herba (GT) or methylparaben (MP) on histopathological changes and 2 biomarkers of oxidative stress in rats subchronicly exposed to bisphenol A (BPA).

METHODSAdult female Wistar rats were orally exposed for 90 d to BPA (50 mg/kg), BPA+GT (35 mg isoflavones/kg) or BPA+MP (250 mg/kg). Plasma and tissue samples were taken from liver, kidney, thyroid, uterus, ovary, and mammary gland after 30, 60, and 90 d of exposure respectively. Lipid peroxidation and in vivo hydroxyl radical production were evaluated by histological analysis along with malondialdehyde and 2,3-dihydroxybenzoic acid detection.

RESULTSThe severity of histopathological changes in liver and kidneys was lower after GT treatment than after BPA or BPA+MP treatment. A minimal thyroid receptor antagonist effect was only observed after BPA+MP treatment. The abnormal folliculogenesis increased in a time-dependent manner, and the number of corpus luteum decreased. No significant histological alterations were found in the uterus. The mammary gland displayed specific estrogen stimulation changes at all periods. Both MP and GT revealed antioxidant properties reducing lipid peroxidation and BPA-induced hydroxyl radical generation.

CONCLUSIONGT L. extract ameliorates the toxic effects of BPA and is proved to have antioxidant potential and antitoxic effect. MP has antioxidant properties, but has either no effect or exacerbates the BPA-induced histopathological changes.

Animals ; Benzhydryl Compounds ; toxicity ; Chemical and Drug Induced Liver Injury ; pathology ; prevention & control ; Endocrine Disruptors ; toxicity ; Female ; Genista ; Hydroxyl Radical ; blood ; Lipid Peroxidation ; drug effects ; Liver ; pathology ; Oxidative Stress ; drug effects ; Parabens ; toxicity ; Phenols ; toxicity ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Rats ; Rats, Wistar