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Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure
1Department Pharmacology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38163, USA. abukiya@uthsc.edu.
Abstract:
Prenatal alcohol exposure results in an array of developmental abnormalities known as fetal alcohol spectrum disorders (FASDs). Despite the high prevalence of FASDs, therapeutic interventions against accidental or intended exposure of developing fetuses to alcohol are limited. This review outlines current knowledge about mitochondria in cerebral blood vessels as a potential target for anti-FASDs intervention. First, it describes the multifaceted role of mitochondria in maintaining the cerebral artery diameter as shown in adult tissue. Second, current literature on alcohol-driven damage of mitochondrial morphology and function in several fetal tissues, including liver, heart, and brain is summarized. The functional consequences of alcohol exposure in these organs include morphological enlargement of mitochondria, increased oxidative stress, and alteration of cellular respiration. These studies point to a tissue-specific effect of alcohol on mitochondrial function and a particular vulnerability of fetal mitochondria to alcohol exposure when compared to adult counterparts. Third, recent work from our group describing persistent changes in fetal baboon cerebral artery proteome following three episodes of prenatal alcohol exposure is reviewed. In conclusion, the consequences of prenatal alcohol exposure on cerebral artery mitochondria constitute an open field of investigation and, eventually, a point of therapeutic intervention against FASDs.
Insights
Mitochondria in fetal cerebral blood vessels are vulnerable to alcohol, causing developmental issues. Targeting these mitochondria may offer new therapies for fetal alcohol spectrum disorders (FASDs).
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Prenatal alcohol exposure causes fetal alcohol spectrum disorders (FASDs), with limited therapeutic options.
- Mitochondria play crucial roles in cellular function and vascular tone.
- Fetal development involves unique sensitivities to environmental factors like alcohol.
Purpose of the Study:
- To review the role of mitochondria in cerebral blood vessels as a potential therapeutic target for FASDs.
- To summarize alcohol's impact on mitochondrial morphology and function in fetal tissues.
- To discuss persistent proteomic changes in fetal cerebral arteries after alcohol exposure.
Main Methods:
- Literature review of mitochondrial function in adult and fetal tissues.
- Analysis of studies detailing alcohol-induced mitochondrial damage.
- Review of proteomic data from baboon models of prenatal alcohol exposure.
Main Results:
- Mitochondria are vital for regulating cerebral artery diameter in adults.
- Alcohol exposure damages fetal mitochondria, causing enlargement, oxidative stress, and altered respiration.
- Fetal mitochondria exhibit greater vulnerability to alcohol than adult mitochondria.
- Prenatal alcohol exposure induces persistent proteomic changes in fetal baboon cerebral arteries.
Conclusions:
- Mitochondria in cerebral blood vessels are a promising, yet understudied, target for anti-FASDs interventions.
- Understanding alcohol's specific effects on fetal mitochondria is key to developing effective therapies.
- Further research into cerebral artery mitochondria could lead to novel therapeutic strategies for FASDs.
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