[11beta-hydroxysteroid dehydrogenase type 2 enzyme activity effect after exposures phthalate esters in maternal]

Area of Science:

• Environmental Health
• Endocrinology
• Developmental Biology

Background:

• Phthalate esters (PAEs) are common environmental contaminants.
• 11beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is crucial for regulating fetal exposure to maternal glucocorticoids.
• Disruptions in 11β-HSD2 activity are linked to adverse fetal development outcomes, including intrauterine growth retardation (IUGR).

Purpose of the Study:

• To investigate the association between maternal urinary phthalate ester metabolites and 11β-HSD2 enzyme activity.
• To explore the potential mechanism by which PAEs might affect fetal development.

Main Methods:

• A case-control study involving 33 newborns with IUGR and 33 normal controls.
• Quantification of four PAE metabolites (MBP, MEHP, MEHHP, MEOHP) and three cortisol metabolites (THF, allo-THF, THE) in maternal urine using high-performance liquid chromatography-tandem mass spectrometry.
• Analysis of the correlation between PAE metabolite concentrations and 11β-HSD2 activity, calculated from urinary cortisol metabolite ratios.

Main Results:

• Elevated urinary concentrations of MBP, MEHHP, MEOHP, and SumDEHP were found in mothers of IUGR infants compared to controls.
• 11β-HSD2 activity was significantly lower in mothers of IUGR infants.
• Maternal urinary concentrations of PAE metabolites were inversely correlated with 11β-HSD2 activity, particularly in mothers of male infants.

Conclusions:

• Phthalate esters (PAEs) exposure in pregnancy may adversely affect fetal development.
• Inhibition of 11β-HSD2 enzyme activity by PAEs is a potential mechanism for these developmental effects.
• These findings highlight the importance of reducing PAE exposure during pregnancy to support healthy fetal growth.