Comparative teratogenicity of triamcinolone acetonide, triamcinolone, and cortisol in the rat

Rowland, Jon M.; Hendrickx, Andrew G.

doi:10.1002/1520-6866(1990)3:4<313::aid-tcm1770030402>3.0.co;2-6

Cited by 10 publications

(5 citation statements)

References 12 publications

(5 reference statements)

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“…In rats, the most severely affected fetal groups have been those treated with doses of 0.5 mg/kg/day or more, on days 12-14 of gestation. 4,5 Fetal growth retardation can be produced at doses below those required to produce malformations. It is apparent that the large increase in the frequency of cleft palate anomalies in our study represents a teratogenic effect.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] In fetal rats, it has been found to have a more potent teratogenic effects than triamcinolone or cortisol. 5 TAC teratogenicity is mainly expressed as intrauterine growth retardation, hypoplastic organs, and malformations like cleft palate. 4,5 Cortisone accelerates physiologic maturation of type II cells and histologic maturation, as shown by the more rapid transition from the glandular to the canalicular stage of lung pulmonary structure.…”

Section: Introductionmentioning

confidence: 99%

“…5 TAC teratogenicity is mainly expressed as intrauterine growth retardation, hypoplastic organs, and malformations like cleft palate. 4,5 Cortisone accelerates physiologic maturation of type II cells and histologic maturation, as shown by the more rapid transition from the glandular to the canalicular stage of lung pulmonary structure. 6,7 A significant increase in the proportion of cells containing osmiophilic granules has been found in fetal lungs exposed to prednisolone 8 or dexamethasone, but this process is preceded by an increase in the volume fraction of saccular airways.…”

Section: Introductionmentioning

confidence: 99%

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Effect of triamcinolone acetonide on the development of the pulmonary airways in the fetal rat

et al. 1997

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Triamcinolone acetonide (TAC) has a potent teratogenic effect on various mammalian fetal tissues as well as a steroid effect on the lung. Less well documented is the fact that it produces profound oligohydramnios. We wished to determine what effect TAC would have on branching morphogenesis and other aspects of lung development, using an in vivo model described previously. Thirty rats were randomized to receive 0.6 mg/kg of TAC or saline on days 12, 13, and 14 of gestation. At gestational days 15, 17, 18, and 21, the left lungs of 365 fetuses were studied by dissecting microscopy, histology, and morphometry. TAC produced profound pulmonary hypoplasia (dry lung weight/body weight 0.025, compared with 0.06 in controls) on day 21. TAC decreased maternal weight gain, fetal weight, placental weight, amniotic fluid, and pole to pole length (PTP), while it increased the peripheral airway count (PAC). The number of central and intermediate airway branches was reduced, and they were dilated. Growth of peripheral airways was enhanced. In treated fetuses epithelial cells lining these airspaces were histologically more mature and the mesenchyme thinner than in controls. These findings were confirmed by the morphometric measurements. We conclude that when TAC is administered in the early phase of fetal rat lung development, the lungs become hypoplastic, with hypoplasia of the intermediate airways, an increase in the number of peripheral airways, and increased differentiation. We speculate that these effects are primarily due to the steroid action of TAC and that the mechanisms of monopodial branching are different from those of dichotomous branching. Pediatr Pulmonol. 1997; 23:76–86. © 1997 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of triamcinolone acetonide on the development of the pulmonary airways in the fetal rat

et al. 1997

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“…In order to investigate the effects of glucocorticoids on secondary palatal shelves in cleft palate in rats, we examined the histopathological and immunohistochemical changes of MEE cells and palatal mesenchymal cells in rat embryos/fetuses prior to or during fusion in the presence of triamcinolone acetonide (TAC) [20], a synthetic glucocorticoid.…”

mentioning

confidence: 99%

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

Furukawa

Usuda

Abe

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. Triamcinolone acetonide (TAC), a synthetic glucocorticoid, induces cleft palate resulting from poor development of palatal shelves in mice. However, TAC has no effect on medial edge epithelial cells (MEE cells) in secondary palatal shelves. In the present study, we examined the relationship between the pathogenesis of cleft palate and the effects on MEE cells and palatal mesenchyma l cells in rat embryos/fetuses exposed to TAC. Pregnant Wistar Hannover rats were given TAC intramuscularly at 0.5 mg/kg at gestation d ays (Day) 12, 13, and 14, then embryos/fetuses were harvested on Days 14.5, 15, 16 and 20. The effects of TAC were as follows; an inhibition of palatal mesenchymal cell proliferation on Day 14.5, a decrease in the density of palatal mesenchymal cells and MEE cells, and expression of epidermal growth factor (EGF) receptors in MEE cells on Day 15, and stratified squamous differentiation of MEE cel ls with expression of cytokeratin and EGF receptors on Day 16. These findings indicated that TAC inhibited the proliferation of mesenchymal cells and affected the differentiation of MEE cells into stratified squamous epithelia in the palatal shelves of rat embryos. H owever, these stratified squamous MEE cells partially fused with each other. Thus, we suspected that a major contributing factor to the formation of TAC-induced cleft palate might not be the altered differentiation of MEE cells, but the inhibition of mesenchymal cell proliferation. KEY WORDS: cleft palate, MEE cell, rat, triamcinolone acetonide, Wistar Hannover.

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“…In another experiment by Rowland and Hendrickx (1983) (Bloom et al, 2001). This study demonstrates that repetitive exposures to maternal betamethasone given female rats during the organogenesis phase of development i.e.…”

Section: Discussionmentioning

confidence: 99%

The ameliorative role of curcumin on the morphological and skeletal malformations induced by betamethasone in rat fetuses

Badawy¹,

Sakr²,

El–Borm³

2018

Egypt. J. Exp. Biol. (Zoo.)

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ABSTRACT:Among the glucocorticoids, betamethasone has become very popular, being more commonly used for several diseases, to promote organ maturation and to prevent preterm delivery. This work aimed to examining the possible morphological and skeletal malformations induced by betamethasone in foetuses of albino rats an d the role of curcumin as antioxidant against these adverse effects. Administration of betamethasone during the organogenesis phase at a dose equivalent to its human counterpart led to severe intrauterine growth retardation relative to the control group as it affected the growth parameters of the foetuses including reduction in length and weight. In addition, various malformations were detected in the skin, head, trunk, limbs and tail. Exencephaly, mandibular hypoplasia, and retarded ossification were the m ost evident endo-skeletal malformations observed in the foetuses maternally injected with betamethasone. A marked improvement in foetal growth in terms of shape, length, weight, and skeleton was recorded in foetuses maternally injected with betamethasone followed by curcumin.

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Comparative teratogenicity of triamcinolone acetonide, triamcinolone, and cortisol in the rat

Cited by 10 publications

References 12 publications

Effect of triamcinolone acetonide on the development of the pulmonary airways in the fetal rat

Effect of triamcinolone acetonide on the development of the pulmonary airways in the fetal rat

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

The ameliorative role of curcumin on the morphological and skeletal malformations induced by betamethasone in rat fetuses

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