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Impact of oxidative stress in fetal programming
Loren P Thompson1, Yazan Al-Hasan
1Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, 11-029 Bressler Research Building, 655 W. Baltimore Street, Baltimore, MD 21201, USA. lthompson@umm.edu
Journal of Pregnancy
|August 1, 2012
Summary
Intrauterine stress can lead to adult diseases via fetal programming. Oxidative stress during development may trigger epigenetic changes, increasing disease risk in offspring.
Area of Science:
- Developmental biology
- Epigenetics
- Reproductive medicine
Background:
- Intrauterine stress is linked to adult disease risk through fetal programming.
- Oxidative stress arises from prenatal hypoxia, nutritional imbalances, and glucocorticoid exposure.
- Oxidant molecules may act as signaling factors in fetal programming.
Purpose of the Study:
- To discuss the role of oxidant molecules in fetal programming.
- To explore epigenetic mechanisms involved in oxidative stress-induced programming.
- To identify therapeutic targets for preventing organ dysfunction in programmed offspring.
Main Methods:
- Review of existing literature on intrauterine stress and fetal programming.
- Analysis of the role of oxidative stress and epigenetic modifications.
- Discussion of potential therapeutic strategies.
Main Results:
- Oxidative stress is a key factor in fetal programming.
- Epigenetic mechanisms mediate the effects of oxidative stress on gene expression.
- Specific target genes are dysregulated by oxidative stress.
Conclusions:
- Oxidative stress during development can program offspring for adult diseases.
- Epigenetic modifications are crucial in mediating these effects.
- Targeting oxidative stress and epigenetic pathways may offer therapeutic benefits.
