Vitamin A Storage in Lungs during Perinatal Development in the Rat

Shenai, Jayant P.; Chytil, Frank

doi:10.1159/000243172

Cited by 64 publications

(48 citation statements)

References 8 publications

(9 reference statements)

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“…In the experiments described above, liver RE was analyzed in parallel with lung RE. As expected from previous studies (26)(27)(28), liver RE concentration exceeded lung RE concentration by z20-fold. However, in contrast to the greater effect of VARA, compared with VA alone, on RE in the lungs, RE in the liver was increased equally by VARA and VA alone (Fig.…”

Section: Histologysupporting

confidence: 89%

“…However, to our knowledge, an oral supplement of VA combined with RA has not been studied previously. VA supplementation alone, given to pregnant rats on gestational day 19, had been shown to increase the RE concentration in the lungs and liver of their fetuses, newborns, and neonates (26)(27)(28). In our studies, VA alone, given directly orally to neonates, also significantly increased the concentration of RE in the lungs and liver (Figs.…”

Section: Discussionsupporting

confidence: 65%

“…Previous studies have characterized the ontogeny of RE storage in the lungs and liver of the perinatal rat (26). In the VA-adequate state, lung RE, mainly as retinyl palmitate, increased between gestational day 14 and 18, then declined abruptly before birth and remained relatively low from day 2 to 21, whereas liver RE increased before birth and increased even higher in the postnatal period (27). The offspring of VA-supplemented mothers showed the same temporal pattern, but their lung and liver RE concentrations were 1.7-to 7.1-fold higher (28).…”

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confidence: 99%

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Vitamin A combined with retinoic acid increases retinol uptake and lung retinyl ester formation in a synergistic manner in neonatal rats

Ross

Ambalavanan

Zolfaghari

et al. 2006

Journal of Lipid Research

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Vitamin A (VA) is stored in tissues predominantly as retinyl esters (REs), which provide substrate for the production of bioactive retinoids. Retinoic acid (RA), a principal metabolite, has been shown to induce postnatal lung development. To better understand lung RE storage, we compared VA (given as retinyl palmitate), RA, and a nutrient-metabolite combination, VARA, given orally on postnatal days 5-7, for their ability to increase lung RE in neonatal rats. VARA increased lung RE significantly [z14, 2.4, 2.1, and ,1 nmol/g for VARA, VA, RA, and control (C), respectively; P , 0.001]; the increase by VARA was more than additive compared with the effects of VA and RA alone. Lung histology and morphometry were unchanged. In a 6 h metabolic study, providing [ In conclusion, VARA, a 10:1 nutrientmetabolite combination, increased lung RE significantly compared with VA alone and could be a promising therapeutic option for enhancing the delivery of VA to the lungs.-Ross, A. C., N. Ambalavanan, R. Zolfaghari, and N-q. Li. Vitamin A combined with retinoic acid increases retinol uptake and lung retinyl ester formation in a synergistic manner in neonatal rats. Retinyl esters (REs) are the most abundant form of vitamin A (VA) in most tissues (1). The hydrolysis of RE generates retinol, which, through oxidative metabolism, yields retinoic acid (RA) (2), a retinoid hormone capable of activating nuclear retinoid receptors and thereby inducing or repressing the transcription of many genes (3-5). Among its many physiological actions, RA regulates cell proliferation, differentiation, and cell-cell interactions (6). For the lungs, retinoids are essential for normal morphogenesis in the fetal period, for maturation and remodeling in the perinatal and postnatal periods, and for maintenance of the fully matured lungs (7-10). In humans, the lungs undergo septation of the thick-walled air saccules in the perinatal period, beginning at approximately week 28 of gestation, with a 2-to 4-fold increase in the gas exchange surface area by weeks 30-40 (7, 11, 12). In rats and mice, septation and the formation of pulmonary alveoli occur mainly in the first 2 weeks of postnatal life (7,10,(12)(13)(14). Whereas a deficiency of dietary VA for 6 weeks resulted in an increased size of rat lung airspaces and reduced elastin in the parenchyma (15), the administration of RA to neonatal rats from postnatal day 3 to 14 increased the septation of the lungs (16,17). RA also attenuated the oxygen-induced inhibition of alveolarization in rats reared during the period of septation in a hyperoxic environment (18). Retinol has shown promise in reducing pulmonary dysfunction in a lamb model of preterm lung injury (19) and in clinical studies of preterm human infants susceptible to bronchopulmonary dysplasia (20)(21)(22)(23)(24)(25).The neonatal rodent is a useful model in which to study the biochemical and morphological development of the lungs in the perinatal period. Previous studies have characterized the ontogeny of RE storage in the lungs and liver...

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Section: Histologysupporting

confidence: 89%

Section: Discussionsupporting

confidence: 65%

mentioning

confidence: 99%

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Vitamin A combined with retinoic acid increases retinol uptake and lung retinyl ester formation in a synergistic manner in neonatal rats

Ross

Ambalavanan

Zolfaghari

et al. 2006

Journal of Lipid Research

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“…At d 17 in fetuses of ethanol-consuming mothers, liver retinol concentrations and total retinol per fetus were elevated and lung retinyl palmitate was greater. From d 17 to 2 1, the normal increase in liver and decrease in lung retinyl palmitate did not occur (23,26). The marked retinol and retinyl palmitate changes in these fetuses suggest that the normal metabolic pathways for vitamin A have been affected by the maternal ethanol consumption.…”

Section: Discussionmentioning

confidence: 88%

The Effect of Maternal Ethanol Ingestion on Fetal Vitamin A in the Rat

Grummer

Zachman

1990

Pediatr Res

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ABSTRACT. The effect of maternal ethanol ingestion on fetal tissue vitamin A was investigated. Pregnant rats were pair-fed control diets or diets containing 36% of energy as ethanol. After 17 or 21 d gestation, fetuses were removed and fetal and maternal tissues were analyzed by HPLC for retinol and retinyl palmitate. Ethanol consumption resulted in fewer fetuses per pregnancy, increased number of resorption~, and increased numbers of gross fetal abnormalities. In maternal tissues, ethanol consumption resulted in greater lung and kidney vitamin A concentrations. In the fetuses of ethanol-consuming pregnancies, free retinol in liver was higher at d 17. However, fetal liver palmitate levels and total retinyl palmitate in liver, lung, and kidney were lower in ethanol-fed rats at d 21 of gestation. Fetal lung retinyl palmitate concentrations were greater at both d 17 and d 21, and kidney levels were also greater at d 21. Ethanol consumption during pregnancy results in an increased incidence of spontaneous abortions (I), an increase in perinatal mortality (2), and a number of congenital malformations (3). The major features of these congenital malformations (FAS) are intrauterine and postnatal growth retardation, craniofacial dysmorphology, congenital heart defects, skeletal anomalies, and CNS dysfunctions (4).Controversy in the literature still exists over the exact mechanism by which ethanol causes FAS. Some believe ethanol and/ or acetaldehyde have a direct teratogenic effect. The other view is that the abnormalities observed are the result of altered maternal or placental physiology or other nutritional deficiencies caused by the ethanol ( 5 , 6).The interaction of ethanol with vitamin A is a complex interaction. It is known that in both man and animals, chronic consumption of ethanol results in very low levels of liver vitamin A reserves. This can occur despite adequate intake and normal plasma levels of this vitamin (7-10). The pattern of fetal anomalies associated with vitamin A deficiency is similar in some respects to that of FAS (1 l), including frequently observed defects of growth, craniofacial, neurologic, urogenital, and heart systems. Therefore, it is conceivable that vitamin A deficiency could be present in FAS.The purpose of our research was to determine if maternal ethanol ingestion had an effect on fetal tissue vitamin A in the rat. We found that fetal vitamin A was significantly decreased in liver, but elevated in lung and kidney. Total vitamin A stores were lower in fetuses born of pregnant dams ingesting ethanol for the 2 1 d of gestation. MATERIALS AND METHODS Alcohol diet and experimental animals. Female timed-preg-nancy Sprague-Dawley rats (Harlan Industries, Indianapolis, IN) were weighed, randomly assigned to groups on d 1 of pregnancy, and kept in individual mesh-bottom cages in a controlled temperature environment with a light-dark cycle of 12 h light, 12 h dark. The rats were fed an isocaloric liquid Lieber-DeCarli diet (Dyets, Inc., Bethlehem, PA) containing 25% protein, 63% carbohydrat...

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“…Therefore during the developmental period of lung growth and differentiation, the storage of lung retinyl esters (mainly retinyl palmitate) may be inadequate because of hydrolysis to retinol. Indeed, the rat lungs stored a large amount of retinyl palmitate in the fetal stages, but the lung was depleted of retinyl esters during perinatal development (5,6).…”

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confidence: 99%

Lack of Lecithin: Retinol Acyltransferase Activity in Chick Lungs.

Takase

Matsumoto

Goda

1996

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryOur previous study revealed that no retinyl esters were detectable in chick and hen lungs, suggesting that the retinol esterification system may be absent in these tissues. This possibility encouraged us to investigate whether chick lungs exhibit the activity of a retinol esterifying enzyme, i.e., lecithin: retinol acyltransferase (LRAT). The LRAT activ ity was assayed with dilauroyl phosphatidylcholine and either complex of retinol-cellular retinol-binding protein, type two or retinol-cellular retinol -binding protein in microsomal preparations of lung, duodenum and liver of 7-day-old chicks. Relatively high levels of LRAT activity were present in the duodenum and the liver of chicks as well as in the rat lung. However, the chick lung exhibited no LRAT activity. The lungs of both rat and chick showed similar and low levels of acyl-CoA: retinol acyl transferase (ARAT) activity, but only rat lung, but not chick lung, contained a detectable amount of retinyl esters. Thus, the retinyl ester storage in the lung seems to depend on the presence of LRAT activity in the lung, but it is independent of the presence of ARAT activity in the lung. The absence of LRAT activity and retinyl esters in the chick lung suggests that the retinol in the chick lung may not be provided from retinyl ester storage, and the retinol transferred directly from serum should be utilized to generate retinoic acid.

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Vitamin A Storage in Lungs during Perinatal Development in the Rat

Cited by 64 publications

References 8 publications

Vitamin A combined with retinoic acid increases retinol uptake and lung retinyl ester formation in a synergistic manner in neonatal rats

Vitamin A combined with retinoic acid increases retinol uptake and lung retinyl ester formation in a synergistic manner in neonatal rats

The Effect of Maternal Ethanol Ingestion on Fetal Vitamin A in the Rat

Lack of Lecithin: Retinol Acyltransferase Activity in Chick Lungs.

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