F&S science最新文献

Objective: To investigate the acute and chronic effects of triclosan (TCS) exposure on ovarian reserve dynamics and reproductive potential in a mouse model.

Design: Female C57BL/6 mice were given a diet containing TCS 10 mg/kg per day or a control diet starting on postnatal day (PND) 30. Ovaries were collected at PND 37, 60, 90, 210, 300, and 360, reflecting 1 week, 1 month, 2 month, 6 month, 9 month, and 12 month periods of exposure. Ovarian follicular compositions were analyzed in both groups at all exposure time points. Animals from both groups at the same exposure time groups were bred with age-matched control C57BL/6 male mice and the number of litters, pups per litter, interlitter interval, and number of deceased pups were recorded.

Subjects: C57BL/6 mice.

Exposure: Triclosan 10 mg/kg per day diet or control diet.

Main outcome measures: Ovarian follicular compositions were analyzed in TCS-treated mice compared with controls at both acute and chronic exposure time points. Animals from both exposure groups were bred and the number of litters, pups per litter, interlitter time interval, and number of deceased pups were analyzed.

Results: Primordial follicle density decreases with age in control and TCS-exposed mice with a trend toward an accelerated decline in the PND 90, 300, and 360 TCS-exposed groups. The TCS-exposed mice at PND 37 and PND 60 both exhibit a trend toward decreased growing follicle (primary and secondary) densities. At PND 300 and 360, there are decreased follicular densities across all follicle types in the TCS-exposed compared with control groups with lower antral follicle densities (0.27 vs. 0.04 at PND 300 and 0.22 vs. 0.06 at PND 360). Litter sizes were similar between groups across all time points. The length of time between first and fifth litters is increased in the TCS-exposed group at PND 37 (116 days vs. 135.2 days), with similar trends seen in the PND 60 (114.7 days vs. 122.8 days) and PND 90 (140.8 vs. 158.8 days) groups, which may suggest longer cycles and reduced rates of ovulation in midreproductive life. No increase in stillbirth was seen in the TCS-exposure groups compared with controls.

Conclusions: Our study demonstrates that TCS exposure may accelerate normal age-related ovarian follicular loss with decreased antral follicle density at chronic exposure timepoints. Triclosan exposure may also impact estrous cycles at midreproductive age.

Objective: To investigate the metabolic alterations at the maternal-fetal interface in missed miscarriage (MM) using untargeted metabolomic and lipidomic profiling of paired villous and decidual tissues.

Design: Observational study utilizing multiomics integration to analyze metabolic and lipidomic profiles.

Subjects: A total of 10 women were recruited in this study, including 5 women with MM and 5 healthy controls. All cases included in the MM group were euploid, excluding chromosomal abnormalities.

Exposure: The exposure in this study was the condition of MM, with tissue samples collected from both villous and decidual tissues.

Main outcome measures: Differentially abundant metabolites and lipids between MM and control groups, focusing on metabolic pathways related to glycerophospholipid metabolism, sphingolipid signaling, and amino acid metabolism.

Results: We identified significant metabolic alterations in both villous and decidual tissues from MM pregnancies compared with healthy controls. Key findings included the downregulation of amino acids and organic acids, such as lactic acid, suggesting impaired energy metabolism. Lipidomic analysis revealed alterations in glycerophospholipids and sphingolipids, indicating disrupted cell signaling and inflammatory pathways in MM.

Conclusion: This multiomics study highlights specific metabolic and lipidomic disruptions in MM, suggesting early metabolic disturbances at the maternal-fetal interface correlate with miscarriage. These findings may guide future therapeutic strategies targeting metabolic pathways to improve pregnancy outcomes in MM.

Objective: To investigate the potential role of butyrylcholinesterase (BChE) enzyme activity and tentative association of BCHE gene single nucleotide polymorphisms (rs3495, rs1803274) with risk of male infertility. Male infertility is a highly prevalent multifactorial condition with complex heterogeneous phenotypic spectrum. A significant global variation has been observed in the prevalence of male infertility contributing to approximately 20%-70% of overall infertility. An interplay of genetic, hormonal, environmental, and lifestyle factors are involved in the development of male infertility. Butyrylcholinesterase, an enzyme involved in oxidative stress and sperm function may play a role in infertility, but its genetic and enzymatic profiles in male infertility are unexplored.

Design: A case-control/observational study was conducted enrolling 55 fertile and infertile male individuals.

Subjects: A total of 55 fertile and infertile male volunteers were included in the study.

Exposure: Volunteers were clinically diagnosed for infertility.

Main outcome measures: Plasma BChE activity was estimated spectrophotometrically by Ellman's method. The single nucleotide polymorphism genotyping of BCHE gene variants was performed by polymerase chain reaction-restriction fragment length polymorphism and tetra-primer amplification refractory mutation system-polymerase chain reaction.

Results: The infertile group exhibited significantly lower BChE activity compared with the fertile group. In addition, a notable genetic association of BCHE variants with the risk of male infertility was identified. The BCHE rs3495 showed significant correlation in the dominant model (odds ratio = 21.67) and allelic distribution (odds ratio = 3.30), whereas rs1803274 showed robust association in all models.

Conclusion: This is the first study linking BCHE variants and reduced BChE enzymatic activity with male infertility. These findings suggest BChE as a potential biomarker and therapeutic target for idiopathic infertility.