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Long term effects of maternal protein restriction on postnatal lung alveoli development of rat offspring
S A Farid, O M Mahmoud1, N A Salem
1Suez Canal University Faculty of Medicine. omima34@hotmail.com.
Insights
Maternal protein restriction during pregnancy impairs neonatal and postnatal lung development in rat offspring. This nutritional deficiency leads to significant morphological and morphometric changes, causing developmental retardation of the lungs.
Area of Science:
- Developmental Biology
- Nutritional Science
- Pulmonology
Background:
- Maternal nutrition significantly impacts fetal growth and organ development.
- Poor nutrition during pregnancy can lead to reduced fetal growth and adverse effects on fetal lung development.
Purpose of the Study:
- To investigate the effects of maternal protein restriction on postnatal lung development.
- To assess the impact on lung structure in adult rat offspring.
Main Methods:
- Pregnant Sprague-Dawley rats were divided into normally nourished and protein-deficient groups.
- Offspring were analyzed at 1 day, 2 weeks, and 2 months postnatal.
- Evaluations included body and lung weight, plasma protein, serum albumin, histology, morphometry, and pulmonary surfactant protein A immunohistochemistry.
Main Results:
- Protein restriction resulted in significant morphological and morphometric changes in lung development.
- Reduced lung weight to body weight ratio was observed in protein-deficient offspring.
- Immunohistochemistry indicated alterations in pulmonary surfactant protein A expression.
Conclusions:
- Maternal protein deficiency interferes with normal neonatal and postnatal lung development.
- Protein deficiency leads to developmental retardation of the lung.
- This highlights the critical role of adequate maternal nutrition for optimal lung development.
Abstract:
Poor nutrition of women during pregnancy causes reduction in foetal growth and can adversely affect the development of the foetal lungs. The purpose of the present study was to assess the effects of maternal protein restriction on the postnatal lung development in neonatal period, and on lung structure in adult rat offspring. Female virgin Sprague-Dawley albino rats (more than 200 g) were used. One male rat was introduced into a cage with one female for matting. Once the pregnancy was confirmed, pregnant rats were divided into two main groups; each consists of 6 female as follow: 1 - normally nourished group; 2 - protein deficient group. After delivery, offspring were subdivided into three groups: 1 day after delivery, 2 weeks and 2 months postnatal. Rat body and lung weight were recorded and ratio of lung weight to body weight was assessed. Total plasma protein and serum albumin were assessed for all groups. Lung tissue stained with H&E for histological and morphometric analysis. Immunohistochemistry was performed to evaluate the number of cells positive for pulmonary surfactant protein A. Our results showed that protein restriction interfere with neonatal and postnatal lung development resulting in morphological and morphometric changes of normal lung development. We concluded that protein deficiency lead to developmental retardation of lung.
