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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
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In utero exposure to benzo(a)pyrene predisposes offspring to cardiovascular dysfunction in later-life

G E Jules1, S Pratap, A Ramesh

  • 1Department of Neuroscience and Pharmacology, Environmental-Health Disparities and Medicine, Center for Molecular and Behavioral Neuroscience, Meharry Medical College, Nashville, TN 37208, USA.

Toxicology
|March 1, 2012
PubMed

Insights

In utero exposure to benzo(a)pyrene (B(a)P) can lead to elevated blood pressure in offspring. This study investigated B(a)P

Area of Science:

  • Environmental Toxicology
  • Developmental Biology
  • Cardiovascular Physiology

Background:

  • Benzo(a)pyrene (B(a)P), a polycyclic aromatic hydrocarbon, is a common environmental pollutant.
  • In utero exposure to B(a)P is suspected to disrupt fetal cardiovascular development.

Purpose of the Study:

  • To investigate the impact of in utero benzo(a)pyrene (B(a)P) exposure on cardiovascular development in Long Evans Hooded (LEH) rat offspring.
  • To identify molecular mechanisms underlying potential B(a)P-induced cardiovascular dysfunction.

Main Methods:

  • Timed-pregnant LEH rats were exposed to varying doses of B(a)P or diluent via oral gavage from embryonic day 14 to 17.
  • Offspring cardiovascular parameters, including systolic blood pressure, were assessed postnatally.
  • Gene expression analysis using microarray and quantitative real-time PCR was performed on cardiovascular tissues.

Main Results:

  • In utero B(a)P exposure did not affect litter size or pre-weaning growth.
  • Offspring exposed to middle and high doses of B(a)P exhibited significantly elevated systolic blood pressure at postnatal day 53.
  • Upregulation of mRNA expression for angiotensin (AngII), angiotensinogen (AGT), and endothelial nitric oxide synthase (eNOS) was observed in exposed offspring.

Conclusions:

  • In utero exposure to benzo(a)pyrene (B(a)P) may predispose offspring to cardiovascular deficits.
  • Elevated systolic blood pressure in B(a)P-exposed offspring is associated with altered expression of key cardiovascular regulatory genes.
  • These findings suggest potential long-term cardiovascular dysfunction resulting from prenatal B(a)P exposure.

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