Postnatal hyperoxia or DEHP exposure leads to growth restriction and delayed lung development in newborn rats
| Autor: | Jing Lin, Bei-Tao Chen, Zhen-lang Lin, Shangqin Chen, Zhong-Jie Liang, Qiu-ping Wu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
endocrine system growth restriction Andrology Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound Random Allocation 0302 clinical medicine Enos Plasticizers newborn Diethylhexyl Phthalate Gene expression medicine Animals Oxygen toxicity Lung Growth Disorders lung development Hyperoxia biology DEHP business.industry Phthalate lcsh:RJ1-570 lcsh:Pediatrics respiratory system medicine.disease biology.organism_classification Rats respiratory tract diseases Oxygen 030104 developmental biology medicine.anatomical_structure 030228 respiratory system chemistry Bronchopulmonary dysplasia Animals Newborn toxic effects Pediatrics Perinatology and Child Health Immunology Room air distribution hyperoxia medicine.symptom business Biomarkers |
| Zdroj: | Pediatrics and Neonatology, Vol 59, Iss 1, Pp 24-30 (2018) |
| ISSN: | 1875-9572 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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