bpa饮水暴露英文文章.doc

1Int J Dev Neurosci. 2011 Feb;29(1):37-43. Epub 2010 Oct 16.Developmental and metabolic brain alterations in rats exposed to bisphenol A during gestation and lactation.Kunz N, Camm EJ, Somm E, Lodygensky G, Darbre S, Aubert ML, Hppi PS, Sizonenko SV, Gruetter R.SourceLaboratory of Functional and Metabolic Imaging (LIFMET), Ecole Polytechnique Fdrale de Lausanne (EPFL), Lausanne, Switzerland.AbstractIn recent years, considerable research has focused on the biological effect of endocrine-disrupting chemicals. Bisphenol A (BPA) has been implicated as an endocrine-disrupting chemical (EDC) due to its ability to mimic the action of endogenous estrogenic hormones. The aim of this study was to assess the effect of perinatal exposure to BPA on cerebral structural development and metabolism after birth. BPA (1mg/l) was administered in the drinking water of pregnant dams from day 6 of gestation until pup weaning. At postnatal day 20, in vivo metabolite concentrations in the rat pup hippocampus were measured using high field proton magnetic resonance spectroscopy. Further, brain was assessed histologically for growth, gross morphology, glial and neuronal development and extent of myelination. Localized proton magnetic resonance spectroscopy (1)H MRS) showed in the BPA-exposed rat a significant increase in glutamate concentration in the hippocampus as well as in the Glu/Asp ratio. Interestingly these two metabolites are metabolically linked together in the malate-aspartate metabolic shuttle. Quantitative histological analysis revealed that the density of NeuN-positive neurons in the hippocampus was decreased in the BPA-treated offspring when compared to controls. Conversely, the density of GFAP-positive astrocytes in the cingulum was increased in BPA-treated offspring. In conclusion, exposure to low-dose BPA during gestation and lactation leads to significant changes in the Glu/Asp ratio in the hippocampus, which may reflect impaired mitochondrial function and also result in neuronal and glial developmental alterations.2J Physiol Biochem. 2011 Jun 9. Epub ahead of printProbable gamma-aminobutyric acid involvement in bisphenol A effect at the hypothalamic level in adult male rats.Cardoso N, Pandolfi M, Lavalle J, Carbone S, Ponzo O, Scacchi P, Reynoso R.SourceLaboratorio de Endocrinologa, Departamento de Fisiologa, Facultad de Medicina Universidad de Buenos Aires, Buenos Aires, Argentina, Paraguay 2155, Piso 7, Buenos Aires, Argentina.AbstractThe aim of the present study was to investigate the effects of bisphenol A (BPA) on the neuroendocrine mechanism of control of the reproductive axis in adult male rats exposed to it during pre- and early postnatal periods. Wistar mated rats were treated with either 0.1% ethanol or BPA in their drinking water until their offspring were weaned at the age of 21days. The estimated average dose of exposure to dams was approximately 2.5mg/kg body weight per day of BPA. After 21days, the pups were separated from the mother and sacrificed on 70day of life. Gn-RH and gamma-aminobutyric acid (GABA) release from hypothalamic fragments was measured. LH, FSH, and testosterone concentrations were determined, and histological and morphometrical studies of testis were performed. Gn-RH release decreased significantly, while GABA serum levels were markedly increased by treatment. LH serum levels showed no changes, and FSH and testosterone levels decreased significantly. Histological studies showed abnormalities in the tubular organization of the germinal epithelium. The cytoarchitecture of germinal cells was apparently normal, and a reduction of the nuclear area of Leydig cells but not their number was observed. Taken all together, these results provide evidence of the effect caused by BPA on the adult male reproductive axis when exposed during pre- and postnatal period. Moreover, our findings suggest a probable GABA involvement in its effect at the hypothalamic level.3Neuro Endocrinol Lett. 2010;31(4):512-6.Evidence to suggest glutamic acid involvement in Bisphenol A effect at the hypothalamic level in prepubertal male rats.Cardoso N, Pandolfi M, Ponzo O, Carbone S, Szwarcfarb B, Scacchi P, Reynoso R.SourceLaboratorio de Endocrinologa, Departamento de Fisiologa, Facultad de Medicina Universidad de Buenos Aires, Buenos Aires, Argentina.AbstractOBJECTIVES: The aim of present paper was to study the probable role of glutamic acid (GLU) as a mediator of bisphenol A (BPA) effect at the hypothalamic level and its effects on the reproductive axis of prepubertal male rats.METHODS: Mated Wistar rats were treated with either 0.1% ethanol (control group, n=10) or BPA (BPA group, n=10) in their drinking water until their offspring were weaned at the age of 21 days. The estimated average dose of exposure to dams was approximately 2.5mg/kg body weight/day of BPA. At the prepubertal stage (35 days of age), the male rats were sacrificed and Gn-RH and glutamic acid (GLU) release, an amino acid involved in Gn-RH secretion, were measured in hypothalamic samples containing medio basal and anterior preoptic area (MBH-APOA), by RIA and HPLC respectively. LH, FSH serum levels were measured by RIA and testosterone by EQLIA.RESULTS: Gn-RH and GLU release decreased significantly in animals exposed to BPA (p0.001, p0.01). LH, FSH and testosterone serum levels were also decreased by treatment (p0.0001).CONCLUSION: Present results provide evidence that BPA may act at the hypothalamic level to decrease GLU release which in turn may modify Gn-RH secretion altering the normal function of the axis.4Environ Health Perspect. 2009 Oct;117(10):1549-55. Epub 2009 Jun 29.Perinatal exposure to bisphenol a alters early adipogenesis in the rat.Somm E, Schwitzgebel VM, Toulotte A, Cederroth CR, Combescure C, Nef S, Aubert ML, Hppi PS.SourceFaculty of Medicine, University of Geneva, Geneva, Switzerland. emmanuel.sommmedecine.unige.chAbstractBACKGROUND: The causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated.OBJECTIVES: The aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning.METHODS: Pregnant Sprague-Dawley rats had access to drinking water containing 1 mg/L BPA from day 6 of gestation through the end of lactation. Pups were weaned on postnatal day (PND) 21. At that time, we investigated perigonadal adipose tissue of pups (weight, histology, gene expression). For the remaining animals, we recorded body weight and food intake for animals on either standard chow or a high-fat diet.RESULTS: Gestational exposure to BPA did not alter the sex ratio or litter size at birth. On PND1, the weight of male and female BPA-exposed pups was increased. On PND21, body weight was increased only in females, in which parametrial white adipose tissue (pWAT) weight was increased about 3-fold. This excess of pWAT was associated with adipocyte hypertrophy and overexpression of lipogenic genes such as C/EBP-alpha (CAAT enhancer binding protein alpha), PPAR-gamma (peroxisome proliferator-activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), LPL (lipoprotein lipase), FAS (fatty acid synthase), and SCD-1 (stearoyl-CoA desaturase 1). In addition, gene expression of SREBP-1C, FAS, and ACC (acetyl-CoA carboxylase) was also increased in liver from BPA-exposed females at PND21, without a change in circulating lipids and glucose. After weaning, perinatal BPA exposure predisposed to overweight in a sex- and diet-dependent manner. We observed no change in food intake due to perinatal BPA exposure in rats on either standard chow or a high-fat diet.CONCLUSIONS: Perinatal exposure to a low dose of BPA increased adipogenesis in females at weaning. Adult body weight may be programmed during early life, leading to changes dependent on the sex and the nutritional status. Although further studies are required to understand the mechanisms of BPA action in early life, these results are particularly important with regard to the increasing prevalence of childhood obesity and the context-dependent action of endocrine disruptors.5J Atheroscler Thromb. 2007 Oct;14(5):245-52. Epub 2007 Oct 12.Perinatal and postnatal exposure to bisphenol a increases adipose tissue mass and serum cholesterol level in mice.Miyawaki J, Sakayama K, Kato H, Yamamoto H, Masuno H.SourceDepartment of Bone and Joint Surgery, Ehime University Graduate School of Medicine, Ehime, Japan.AbstractAIM: To investigate whether the perinatal and postnatal exposure of mice to bisphenol A (BPA) caused the development of obesity and/or hyperlipidemia.METHODS: Pregnant mice were exposed to BPA in drinking water at concentrations of either 1 microg/mL (LD group) or 10 microg/mL (HD group) from gestation day