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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Perinatal Lead (Pb) Exposure Increases Mouse Embryonic Weight and Alters Neuronal Gene Expression
Bambarendage P U Perera1,2, Minghua Li3, Anagha Tapaswi1
1Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI 48109, USA.
Insights
Perinatal lead (Pb) exposure in mice increased embryonic weight and altered gene expression, particularly in imprinted, X-linked, and sexually dimorphic genes. These changes may impact long-term neurodevelopment and health outcomes.
Area of Science:
- Environmental Health
- Developmental Biology
- Toxicology
Background:
- Prenatal and early-life lead (Pb) exposure is associated with adverse neurodevelopmental outcomes in children.
- The specific molecular mechanisms by which Pb exposure affects embryonic development and long-term health are not fully understood.
Purpose of the Study:
- To investigate the impact of perinatal lead exposure on gene expression patterns in mouse embryos.
- To identify specific gene categories, including imprinted, X-linked, and sexually dimorphic genes, affected by lead exposure.
- To explore potential pathways linking lead exposure to later-life health issues.
Main Methods:
- Female mice received lead acetate in drinking water before and during early pregnancy.
- Embryos were collected at embryonic day (E)10-12, weighed, and sexed.
- RNA sequencing was performed on a subset of embryo heads (n≥9 per sex per group).
- Linear regression analysis was used to assess the effects of lead on embryonic weight and gene expression, stratified by sex.
Main Results:
- Lead-exposed embryos exhibited increased weight compared to controls (p=0.007).
- A total of 2,920 differentially expressed genes (FDR<0.05) were identified, including 31 imprinted and 120 X-linked genes.
- Lead exposure altered the expression of genes involved in neuronal structure and function.
- Sexually dimorphic gene expression was affected, with 44 genes altered in females and 76 in males.
Conclusions:
- Perinatal lead exposure significantly alters embryonic gene expression, impacting critical gene categories.
- Changes in imprinted, X-linked, and sexually dimorphic gene expression pathways may underlie lead-induced neurodevelopmental and long-term health effects.
- These findings provide molecular insights into the developmental toxicity of lead exposure.
Abstract:
Acute and chronic exposure to lead (Pb) during pregnancy is linked to adverse health outcomes, including delayed neurodevelopment in offspring. However, the pathways by which Pb exposure influences long-term health remain poorly understood. To address this, we measured the effects of perinatal Pb exposure on gene expression including imprinted genes, X-linked genes, and sexually dimorphic genes. Female mice were given control or Pb acetate dosed (32 ppm) drinking water two weeks prior to timed mating until embryonic day (E)10-12, upon which whole embryos were collected, weighed, and sexed at E13-15. From a subset of embryo heads (n≥9 per sex per group), we extracted and sequenced RNA. We used linear regression to assess Pb impacts on embryonic weight and gene expression across all mice and stratified by sex. Among the differentially expressed genes, we identified significantly enriched pathways. Pb-exposed embryos weighed more than controls (p=0.007), across both sexes. Collectively, we identified 2,920 differentially expressed genes (FDR<0.05), including 31 imprinted genes and 120 X-linked genes upon Pb exposure. Pb exposure altered expression in gene pathways related to neuronal structure and function as well as sexually dimorphic genes (44 for females; 76 for males). These findings highlight perinatal Pb-linked alterations that may drive later-life health outcomes.
