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[Gene expression patterns of offsprings' hepatocytes induced by prenatal Benzo[a]pyrene exposure]
1Institute for Environmental Health and Related Product Safety, Chinese Center for Disease Control and Prevention, Beijing 100021, China.
Insights
Prenatal exposure to Benzo[a]pyrene (BaP) alters offspring liver gene expression, impacting growth and development. Key genes and signaling pathways involved in BaP toxicity were identified, offering insights into developmental risks.
Area of Science:
- Toxicology
- Developmental Biology
- Genomics
Context:
- Benzo[a]pyrene (BaP) is a common environmental pollutant.
- Prenatal exposure to toxicants can have long-lasting effects on offspring health.
- Understanding the molecular mechanisms of BaP toxicity is crucial for risk assessment.
Purpose:
- To investigate the impact of prenatal Benzo[a]pyrene (BaP) exposure on gene expression in infant rat livers.
- To identify key genes and signaling pathways involved in BaP-induced toxicity during development.
Summary:
- Prenatal BaP exposure in rats led to significant changes in offspring liver gene expression, with 1232 differentially expressed genes identified.
- Gene expression patterns varied with BaP dosage, affecting pathways related to growth, development, toxicant metabolism, and inflammation.
- Key genes such as CYP2C13, GSTO1, Rela, MAPK8, and Plcg1 were implicated in the toxicological network.
Impact:
- Provides novel insights into the molecular mechanisms underlying prenatal BaP toxicity.
- Highlights potential risks to offspring growth and development following maternal exposure.
- Identifies critical genes and pathways for future research and potential intervention strategies.
Objective:
To study the gene expression patterns in livers of infant rats after Benzo[a]pyrene (BaP) exposure during pregnancy and explore the important gene and signaling pathways in the toxic mechanism of BaP.
Methods:
Thirty-two pregnant SD rats were randomly divided into four groups: vehicle control (corn oil) and treatment groups (0.75, 1.50 and 3.00 mg/kg BaP in corn oil). BaP solutions were given by gastric infusion from the 3rd to the 17th day of pregnancy. After delivery the offspring's liver were taken to detect the gene expression by RatRef-12 gene chip. The stability of gene chip was tested by repeated experiments.
Results:
After prenatal BaP exposure 1232 genes with different expression variations in hepatocytes of offsprings were identified. Three expression patterns of genes related to the dose of prenatal BaP exposure were identified with significant difference (P < 0.05). As the dose of prenatal BaP exposure increased, the gene expression patterns were downregulated, upregulated, and fluctuated. Twenty-six signaling pathways with differently expressed genes mainly focused on: growth and development, toxicant metabolism and inflammation (P < 0.05). The data from gene network analysis demonstrated that CYP2C13, GSTO1, Rela, MAPK8 and Plcg1 were the key genes in the gene network.
Conclusion:
Gene expression patterns of offsprings' hepatocytes were influenced by prenatal BaP exposure. Some key genes and signal pathways were also found. The study provides an important clue for the toxicity and mechanisms of the prenatal BaP exposure on the growth and development of offspring.
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