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Parental Alcohol Exposures Associate with Lasting Mitochondrial Dysfunction and Accelerated Aging in a Mouse Model.

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Parental alcohol exposure leads to premature cellular aging in offspring, impacting mitochondrial function and potentially contributing to fetal alcohol spectrum disorders (FASDs) and accelerated aging.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Gerontology

Background:

  • Fetal alcohol exposure causes mitochondrial dysfunction.
  • Long-term effects of this dysfunction into adulthood and links to accelerated aging in FASDs are unknown.

Purpose of the Study:

  • Investigate if parental alcohol exposure induces premature cellular senescence and accelerated aging in adult offspring.
  • Examine the impact of maternal, paternal, and dual-parental alcohol exposure on age-related outcomes.

Main Methods:

  • Utilized a multiplex preclinical mouse model.
  • Assessed markers of cellular senescence and age-related outcomes in adult offspring (postnatal day 300).
  • Analyzed mitochondrial function, NAD+/NADH ratio, and SIRT1/SIRT3 expression.

Main Results:

  • Adult offspring of alcohol-exposed parents showed increased cellular senescence markers in the brain and liver.
  • Dual-parental alcohol exposure in males exacerbated age-related liver disease indicators more than single-parent exposure.
  • Chronic parental alcohol use resulted in enduring mitochondrial dysfunction, reduced NAD+/NADH ratio, and altered SIRT1/SIRT3 expression.

Conclusions:

  • Parental alcohol use can program offspring for accelerated aging via mitochondrial dysfunction.
  • This accelerated aging may contribute to certain aspects of fetal alcohol spectrum disorders (FASDs).
  • Enduring changes in mitochondrial bioenergetics and NAD+ metabolism are implicated.