Adipogenic effects of prenatal exposure to bisphenol S (BPS) in adult F1 male mice.

Bisphenol S (BPS) has been increasingly used as a substitute for bisphenol A (BPA), a known endocrine disruptor. Early-life exposure to BPA affects fetal development and the risk of obesity in adolescence and adulthood. However, the effects of fetal exposure BPS in later life are unknown. This study aimed to investigate the effects of prenatal BPS exposure on adiposity in adult F1 mice. Pregnant C57BL/6 N mice were exposed to BPS (0, 0.05, 0.5, 5, and 50 mg/kg/d) via drinking water from gestation day 9 until delivery. Thereafter, two groups of offspring (6 weeks old) were either administered a standard diet (STD) or a high-fat diet (HFD) for 4 weeks until euthanasia. The body weight and gonadal white adipose tissue (gWAT) mass were determined, and the energy expenditure for the adiposity phenotype was computed especially for male mice, followed by histological analysis of the gWAT. Thereafter, the expression levels of adipogenic marker genes (Pparg, Cebpa, Fabp4, Lpl, and Adipoq) were analyzed in the gWAT via reverse-transcription PCR analysis. BPS-exposed male mice displayed apparent gWAT hypertrophy, consistent with the significant increase in adipocyte size in the gWAT and upregulation of Pparg and its direct target genes among HFD mice in comparison with the control mice. These results suggest that prenatal BPS exposure potentially increases the susceptibility to HFD-induced adipogenesis in male adult mice.

Bisphenol A in infant urine and baby-food samples among 9- to 15-month-olds.

Diet is the predominant source of bisphenol A (BPA) intake, but limited data are available on BPA levels in the diet of younger infants. This study investigated BPA levels in baby-food and urine samples collected from young infants (under 2 years old). Samples of homemade baby food (n = 210) and urine (n = 187) were collected at 9, 12, and 15 months after birth from a panel of Korean infants (n = 173). BPA levels in urine and food were measured using HPLC-MS/MS and GC-MS, respectively. BPA was above the limit of detection (LOD) in 85.5-85.7% of the urine samples and 32.5-76.3% of the baby-food samples. The median levels of BPA were 0.45 ng/g wet weight (IQR: not detectable to 5.16 ng/g wet weight) in homemade baby food, 0.93 µg/L (IQR:

Pharmacokinetics of bisphenol S in humans after single oral administration.

Bisphenol S (BPS) has been introduced as a substitute for bisphenol A (BPA), and widely used in the manufacture of polycarbonate plastics, epoxy resins and thermal papers. Despite its adverse health outcomes and widespread exposure, pharmacokinetic data of BPS are not available for either animals or humans. The objective of the study is to describe pharmacokinetic characteristics of BPS in human body after a single oral administration with a compartmental pharmacokinetic model. Seven healthy young adults were orally exposed to 8.75µg/bw of d4-BPS, and serum and urine samples were collected for 48h. The concentrations of total and unconjugated d4-BPS in samples were measured using HPLC-MS/MS. Based on the time-concentration profiles in serum and urine, non-compartmental analysis was performed, and two-compartment model was constructed and validated. As a result of non-compartmental analysis, total d4-BPS was rapidly absorbed within 1h (0.7±0.3h) after oral administration, and excreted in urine with terminal half-life of <7h (6.8±0.7h). Fractional urinary excretion (Fue) of total d4-BPS for 48h was 92±17% (67-104%) for men and 70±36% (59-77%) for women. The two-compartment model well described pharmacokinetic properties of BPS, and its parameter estimates were consistent with those from non-compartmental analysis. This study provides information on absorption, distribution, metabolism and elimination of BPS in human body, and the pharmacokinetic model can be utilized for estimating exposure dose of BPS, contributing to more realistic exposure assessment.