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Postnatal hyperoxia or DEHP exposure leads to growth restriction and delayed lung development in newborn rats
Zhong-Jie Liang1, Qiu-Ping Wu1, Bei-Tao Chen2
1Department of Neonatal Intensive Care Unit, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Zhejiang, China.
Insights
Di-(2-ethylhexyl) phthalate (DEHP) and hyperoxia exposure in newborn rats caused growth restriction and delayed lung development. Vascular Endothelial Growth Factor (VEGF) gene expression was altered, suggesting a role in these developmental issues.
Area of Science:
- Neonatal Physiology
- Toxicology
- Pulmonary Medicine
Background:
- Di-(2-ethylhexyl) phthalate (DEHP) is a common plasticizer in medical devices.
- Maternal DEHP exposure has been linked to restricted growth and delayed lung maturation in offspring.
- Oxygen toxicity is a significant risk factor for bronchopulmonary dysplasia.
Purpose of the Study:
- To investigate the effects of hyperoxia, DEHP, or a combination of both on newborn rat growth and lung maturation.
- To understand the impact of these exposures on lung development and molecular markers.
Main Methods:
- Newborn rats were exposed to DEHP, hyperoxia, or both for one to two weeks.
- A control group received vehicle and room air.
- Lung development was assessed by radial alveolar count.
- Gene expression of VEGF, VEGFR-2, and eNOS was analyzed using quantitative RT-PCR.
Main Results:
- Hyperoxia and combined hyperoxia+DEHP exposure caused growth failure.
- Hyperoxia-exposed pups showed catch-up growth, but not those continuously exposed to DEHP.
- Both hyperoxia and DEHP delayed lung development, indicated by reduced radial alveolar counts.
- Hyperoxia decreased VEGF, VEGFR-2, and eNOS transcripts; DEHP alone decreased VEGF expression.
Conclusions:
- Postnatal exposure to hyperoxia and/or DEHP results in growth restriction and impaired lung alveolar development.
- Altered Vascular Endothelial Growth Factor (VEGF) gene expression is implicated as a potential molecular mechanism.
Background:
Di-(2-ethylhexyl) phthalate (DEHP) is commonly used as a plasticizer in many medical devices. We previously showed that maternal DEHP exposure led to restricted growth and delayed lung maturation in newborn rats. As oxygen toxicity continues to be a major risk factor for bronchopulmonary dysplasia, the aim of this study was to examine the effect of hyperoxia, DEHP or DEHP combined with hyperoxia on the growth and lung maturation of newborn rats.
Methods:
Newborn rats received DEHP injection, hyperoxia exposure or DEHP injection combined with hyperoxia exposure for one week or two weeks. A control group received an equal volume of vehicle and was maintained in room air.
Results:
Hyperoxia and hyperoxia + DEHP exposure for one week led to growth failure in newborn rats. Pups in the hyperoxia group showed catch-up growth after being maintained in room air for an additional 7 days but this was not the case with the latter group, which continued to receive DEHP. Hyperoxia and DEHP both delayed lung development, as evidenced by decreased radial alveolar count. Quantitative RT-PCR showed that hyperoxia decreased the transcripts of VEGF, VEGFR-2 and eNOS on days 7 and 14, and DEHP exposure alone also led to decreased expression of VEGF gene in 14-day-old rat pups.
Conclusion:
Postnatal hyperoxia and/or DEHP exposure lead to growth restriction and delayed lung alveolar development. The VEGF gene expression was altered and may be involved as one of the possible molecular mechanisms.
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