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Ethanol Exposure Increases Oxygen Consumption by Developing Cerebral Arteries in a Trimester-, Concentration- and

Shiwani Thapa1, Rika M Morales1, Heather S Smallwood2

  • 1Department of Pharmacology, Addiction Science and Toxicology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38103, USA.

Biomolecules
|November 27, 2025
PubMed

Insights

Prenatal ethanol exposure can harm fetal brain development. Heavy alcohol consumption during the third trimester equivalent significantly altered mitochondrial function in developing cerebral arteries, with sex-specific effects observed.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Prenatal ethanol exposure (PEE) is a leading cause of fetal alcohol spectrum disorders (FASDs).
  • Cerebral circulation is a known target of PEE, but specific mechanisms remain unclear.
  • Mitochondrial function is crucial for vascular smooth muscle contractility and may be affected by alcohol.

Purpose of the Study:

  • To investigate the impact of PEE on mitochondrial function in developing cerebral arteries.
  • To determine if ethanol's effects are dependent on developmental stage and sex.
  • To explore the role of corticosterone in PEE-induced cerebrovascular changes.

Main Methods:

  • Pregnant mice received varying doses of ethanol during second or third trimester equivalents.
  • Measured maternal/progeny blood ethanol, progeny brain weight, cerebral artery oxygen consumption, and corticosterone.
  • Assessed mitochondrial respiratory parameters in developing cerebral arteries.

Main Results:

  • Low ethanol doses (3-4.5 g/kg) showed no significant effect on fetal cerebral artery mitochondrial function.
  • High ethanol dose (6 g/kg) during the third trimester equivalent significantly increased mitochondrial respiration.
  • Sex-specific dimorphism in cerebrovascular response was observed at this stage.
  • Corticosterone levels were not elevated in fetuses or pups.

Conclusions:

  • Cerebrovascular oxygen consumption exhibits developmental stage- and sex-dependent vulnerability to ethanol exposure.
  • Heavy maternal ethanol consumption during late gestation critically impacts mitochondrial function in developing cerebral arteries.
  • These findings highlight specific windows of vulnerability for PEE on the developing brain vasculature.

Keywords:
Seahorsealcohol in uteromaternal drinkingmitochondriarespiratory chain

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