Background: In recent years, fatty acid ethyl esters (FAEEs) in meconium emerged as reliable, direct biological markers for establishing gestational ethanol exposure. Among the minor nonoxidative products of ethanol metabolism, there are ethyl glucuronide (EtG) and ethyl sulfate (EtS).
Objectives: The aim of the study was to analyse meconium specimens from two different Mediterranean cohorts to check for the presence of EtG and EtS, and to investigate the eventual correlation between meconium FAEEs and these two metabolites and their possible application as direct biomarkers of gestational ethanol exposure.
Methods: FAEEs, EtG and EtS were quantified by liquid chromatography tandem mass spectrometry in meconium samples obtained from the Neonatal Intensive Care Unit of Arcispedale Santa Maria Nuova, Reggio Emilia, Italy (N= 96) and from the Pediatric Service of the Hospital del Mar in Barcelona, Spain (N=81).
Results: EtG was present in more than 80% meconium samples while EtS only in 50% specimens Although the samples from Spain and Italy originated from similar socio-demographic cohort, EtG values in the Barcelona samples (median value: 101.5 ng/g) were statistically higher than those from Reggio Emilia ones (median value: 15.6 ng/g). In the Barcelona cohort, EtG values could differentiate between samples with FAEEs below and those equal or above 2 nmol/g - the cut-off used to differentiate heavy maternal ethanol consumption during pregnancy from occasional or no use.
Conclusion: For the first time the presence of EtG and EtS in meconium has been proven, with EtG concentration likely to discriminate heavy maternal ethanol consumption during pregnancy disclosed by FAEEs concentration in this matrix. Further investigations are needed to verify the use of these two ethanol metabolites as alternative biomarkers of chronic in utero exposure to ethanol.
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Neuropharmacology
December 2024
Department of Psychology, Center for Development and Behavioral Neuroscience, Binghamton University, Binghamton NY 13902, United States; Developmental Exposure Alcohol Research Center, Binghamton NY 13902, United States. Electronic address:
Individuals with prenatal alcohol exposure (PAE) are at a higher risk for developing alcohol use disorder (AUD). Using a rat model of moderate PAE (mPAE) on gestational day 12 (G12; ∼2 trimesters in humans), a critical period for amygdala development, we have shown disruptions in medial central amygdala (CeM) function, an important brain region associated with the development of AUD. In addition to this, acute ethanol (EtOH) increases GABA transmission in the CeM of rodents in a sex-dependent manner, a mechanism that potentially contributes to alcohol misuse.
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Department of Physiology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil.
It is known that adverse stimuli, such as altered diets during pregnancy and lactation can result in deleterious effects on the progeny. The aim of this study was to evaluate the possible gastrointestinal repercussions in the offspring of Wistar rats exposed to high-fat diets. Pregnant rats were divided into three groups: normolipidic diet (3.
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November 2024
Department of Pediatrics, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Prenatal alcohol exposure (PAE) is associated with long-term neurodevelopmental deficits resulting in impaired executive functioning and motor control. Intriguingly, PAE has been linked with an increased risk of transient systemic hypoxia-ischemia (TSHI), which alone results in suboptimal fetal growth and neurodevelopmental consequences. Here, using two translationally relevant preclinical models, we investigated the short-term and lasting effects of PAE and TSHI on the morphology of the medial prefrontal cortex (mPFC), a region important in executive function, and tested whether PAE interacts with TSHI to produce a distinct pattern of injury relative to either condition alone.
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December 2024
State Key Laboratory of Experimental Hematology, the Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Key Laboratory of Medical Epigenetics, Department of Cell Biology, Tianjin Medical University, Qixiangtai Road 22, Tianjin 300070, China; Tianjin Key Laboratory of Epigenetics for Organ Development of Premature Infants, Tianjin 300450, China. Electronic address:
Unintentional, early pregnancy alcohol consumption affects embryonic development. During the peri-implantation stage, coinciding with the transition from naive to primed pluripotency, the long isoform of KDM2B (KDM2BLF) underlies the de novo establishment of polycomb repressive complex (PRC) functions at promoters after fertilization. However, it remains unclear whether and how ethanol exposure affects this spatiotemporal chromatin setting.
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November 2024
Serbsky National Medical Research Center of Psychiatry and Narcology, Ministry of Health of the Russian Federation, Moscow, 119002, Russia.
Neuroinflammation can be an important factor of many disorders in central nervous system (CNS) including cognitive dysfunction, affective disorders, and addictive behavior associated with prenatal alcohol exposure and presented in early adulthood. In this study we used an experimental rodent model of prenatal alcohol (PA) exposure (consumption of a 10% ethanol solution by female Wistar rats throughout pregnancy), multiplex immunofluorescence analysis of interleukins (IL-1α, IL-1β, IL-3, IL-6, IL-9, and IL-12), tumor necrosis factor (TNF-α), and chemokine CCL5, as well as quantitative real-time PCR to assess the level of cytokine mRNAs in the prefrontal cortex of the sexually mature (PND60) offspring - male and female rats with prenatal alcohol intoxication and control animals. Significant decrease in the content of TNF-α and interleukins IL-1β, IL-3, IL-6, IL-9 was detected in the prefrontal cortex of male, but not in the female PA offspring.
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