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.
Highlights
Alcohol is one of the most widely consumed psychoactive substances in the world [1]
We focused on nonhuman primates, which offer several advantages to work on fetal alcohol spectrum disorders (FASDs)-related questions
While we cannot evaluate every possible aspect of arterial basic function, it is function plays a critical role in cellular recovery from ischemia/reperfusion [102,115,116,117], the role of mitochondria capacity to cope with the environmental stress following prenatal alcohol exposure should be explored systematically
Summary
Alcohol (ethyl alcohol, ethanol) is one of the most widely consumed psychoactive substances in the world [1]. As documented by numerous studies, maternal alcohol consumption with sharp and high peaks of maternal blood alcohol levels (BAL) above 80 mg/dL poses the highest risk of fetal developmental abnormalities [4,5,6]. These abnormalities encompass multiple aspects of fetal development, ranging from subtle cognitive delay to severe morphological and neuronal anomalies. The effects of alcohol on fetal cerebrovascular function started receiving increasing attention, as brain energetic demands are usually met by a constantly adapting blood supply [20]. The review concludes with the prospective view on the future of cerebrovascular mitochondria research in the field of FASD pathology and therapeutic developments
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