Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood

Abstract

Prenatal alcohol exposure (PAE) can have immediate and long-lasting toxic and teratogenic effects on an individual’s development and health. As a toxicant, alcohol can lead to a variety of physical and neurological anomalies in the fetus that can lead to behavioral and other impairments which may last a lifetime. Recent studies have focused on identifying mechanisms that mediate the immediate teratogenic effects of alcohol on fetal development and mechanisms that facilitate the persistent toxic effects of alcohol on health and predisposition to disease later in life. This review focuses on the contribution of epigenetic modifications and intercellular transporters like extracellular vesicles to the toxicity of PAE and to immediate and long-term consequences on an individual’s health and risk of disease.

The high-expression programming of SR-B1 mediates adrenal dysfunction in female offspring induced by prenatal caffeine exposure and its cholesterol accumulation mechanism

“…Many studies have suggested that epigenetic modification is involved in the abnormal development of multiple organs in offspring exposed to adverse environments during pregnancy. [61][62][63] For example, prenatal dexamethasone exposure could inhibit the H3K27ac level and expression of adrenal IGF1 via the GRα/miR-370-3p/Sirt3 pathway, and programmed the adrenal hypofunction of offspring. 64 In this study, we found that the level of H3K14ac in the promoter region of SR-B1 of the PCE female offspring increased consistently before and after birth.…”

Maternal risk factors for fetal alcohol spectrum disorders: Distal variables

“…Beyond the proximal risk factors of prenatal use of alcohol and other teratogenic drugs, many other variables contribute to the variation and severity of child outcomes. Certainly, genetic and epigenetic traits of both the father and mother (Chung et al, 2021;Thomas et al, 2023) play a role in outcome and trait severity; but multiple other, more distal factors, also contribute to phenotypic variation (McQuire et al, 2020;Montag, 2016;Roozen et al, 2018).…”

“…Beyond the proximal risk factors of prenatal use of alcohol and other teratogenic drugs, many other variables contribute to the variation and severity of child outcomes. Certainly, genetic and epigenetic traits of both the father and mother (Chung et al., 2021; Thomas et al., 2023) play a role in outcome and trait severity; but multiple other, more distal factors, also contribute to phenotypic variation (McQuire et al., 2020; Montag, 2016; Roozen et al., 2018). A pregnant woman's nutritional status has been proven influential, for multiple nutritional deficiencies have been associated with more dysmorphia, cognitive and behavioral delays, and growth restriction (Carter et al., 2017; Huebner et al., 2015; May et al., 2014; Wozniak et al., 2015; Zeisel, 2009).…”

Mechanism of leptin-NPY on the onset of puberty in male offspring rats after androgen intervention during pregnancy

“…With the development of ‘Fetal Origin of Adult Disease’ (FOAD) and ‘Development Origin of Health and Disease’ (DOHaD) ( 11 , 12 ), an increasing number of studies have linked the endocrine environment during pregnancy to the long-term effects on future generations ( 13 – 16 ). With lifestyle changes and the effects of exogenous endocrine disruptors ( 17 ), the proportion of women with high androgen levels during pregnancy was significantly increased ( 18 – 20 ).…”