Renal anomalies in the fetal alcohol syndrome

DeBeukelaer, Martin M.; Randall, Carrie L.; Stroud, Donna R.

doi:10.1016/s0022-3476(77)81033-0

Cited by 42 publications

(15 citation statements)

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“…Hypoplasia and malformations of different organs are described both clinically and experimentally in the FAS (8,15,23,30).…”

Section: Fas Fetal Alcohol Syndromementioning

confidence: 99%

“…Compared to controls, ethanol fetuses had reduced body weight (21%), lung dry weight (39%), lung wet weightlbody weight ratio (lo%), DNA (21%), RNA (25%), protein (28%), and protein/DNA ratio (8%) ( p < Prenatal ethanol exposure results in a spectrum of growth disturbances known as the FAS and includes intrauterine and postnatal growth retardation, facial dysmorphogenesis, and CNS dysfunction (30). Hypoplasia and malformations of different organs are described both clinically and experimentally in the FAS (8,15,23,30).Children with the FAS have an increased frequency and severity of lower respiratory tract infections, which have been previously attributed to immunologic deficiencies induced prenatally by ethanol (19). In addition, decreased production of lung surfactant, decreased activity of pulmonary alveolar macrophages and cilia, and impaired migration of polymorphonuclear leukocytes to the lung occur with ethanol exposure in the adult (2, 13, 14, 31).…”

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Effect of Intrauterine Ethanol Exposure on Fetal Lung Growth

et al. 1985

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ABSTRAm. Lung weight, DNA, RNA, protein, and total body weight were analyzed in fetuses from 14 pregnant Sprague-Dawley rats fed a nutritionally complete liquid diet containing v/v 6% ethanol (ethanol group). Each ethanol rat was matched with an isocalorically pair-fed animal (control group) who received the same liquid diet with carbohydrate substituted for ethanol. The rats were killed on day 20 of gestation. The mean maternal blood ethanol concentration at 0700 h on day 20 was 170 2 22 (SE) mg/dl. Compared to controls, ethanol fetuses had reduced body weight (21%), lung dry weight (39%), lung wet weightlbody weight ratio (lo%), DNA (21%), RNA (25%), protein (28%), and protein/DNA ratio (8%) ( p < Prenatal ethanol exposure results in a spectrum of growth disturbances known as the FAS and includes intrauterine and postnatal growth retardation, facial dysmorphogenesis, and CNS dysfunction (30). Hypoplasia and malformations of different organs are described both clinically and experimentally in the FAS (8,15,23,30).Children with the FAS have an increased frequency and severity of lower respiratory tract infections, which have been previously attributed to immunologic deficiencies induced prenatally by ethanol (19). In addition, decreased production of lung surfactant, decreased activity of pulmonary alveolar macrophages and cilia, and impaired migration of polymorphonuclear leukocytes to the lung occur with ethanol exposure in the adult (2, 13, 14, 31). Received February 10, 1984: accepted July 11, 1984. Send correspondence and reprint requests to Laura S. Inselman, M.D., Department of Pediatrics, North Shore University Hospital, 300 Community Drive, Manhasset, NY 11030.Supported in part by a grant ROI-HD 17375 from the NICHD. S.E.F. is the recipient of a Research Scientist Development Award KO2 AA00074 from the NIAAA. Vol. 19, No. 1, 1985 Printed in U.S.A.Ethanol may also affect the growth and development of the lung. Since lung growth is characterized by the formation of all pulmonary airways and air spaces during gestation (18,22), intrauterine ethanol exposure may alter prenatal lung growth and predispose the lung to the future development of disease. Therefore, the effect of chronic prenatal ethanol ingestion on fetal lung growth was studied in rats. MATERIALS AND METHODSEight mature female Sprague-Dawley rats (ethanol group) were acclimated over 10 days to a nutritionally complete liquid diet, modified for pregnancy with additional vitamins and minerals (Lieber-DeCarli; BioServ Inc, Frenchtown, NJ). The ethanol diet contained v/v 2% ethanol for 3 days, 4% for 3 additional days, and 6% thereafter. Each ethanol rat was matched with an isocalorically pair-fed animal (control group) who received the same liquid diet with carbohydrate substituted for ethanol. Both liquid diets have a caloric density of 1 cal/ml with 18 and 35% of the calories provided by protein and fat, respectively. Ethanol provides approximately 35% of the calories in the 6% ethanol diet.During the mating period the liquid diets were disco...

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“…Hypoplasia and malformations of different organs are described both clinically and experimentally in the FAS (8,15,23,30).…”

Section: Fas Fetal Alcohol Syndromementioning

confidence: 99%

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confidence: 99%

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Effect of Intrauterine Ethanol Exposure on Fetal Lung Growth

et al. 1985

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“…Consumption of alcoholic beverages during pregnancy is the main known cause of congenital anomalies, the fetal alcohol síndrome being one of the major consequences of its utilization during pregnancy. It occurs in approximately 2.2 of every 1000 live new-born, that present a specific pattern of congenital malformations including retardation of pre-and post-natal growth, facial dimorphism, ptosis, strabismus, short palpebral fissures, member anomalies, central nervous system dysfunction (Clarren & Smith, 1978) (Jones et al, 1973;Jones & Smith, 1975;Hanson et al, 1976;Peiffer et al, 1979), and of neural tube (Goldstein & Arulanantham, 1978) and renal anomalies (DeBeukelaer et al, 1977;Goldstein & Arulanantham;Pfeiffer et al).…”

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confidence: 99%

Histometric Study of the Epithelium of Rats Submitted to Ethanol During Lactation

et al. 2007

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SUMMARY:The present work studied the adverse effects of maternal exposure of rats to alcohol during lactation, on the development of their offspring. Histometric evaluation by karyometry and of the palatine epithelium of the sucking was performed. Two groups of animals, one coming from mothers exposed to drinking water containing 20% ethanol during the total lactation period and the other of controls coming from mothers receiving only alcohol-free drinking water during this period. On the 21 first day of lactation the young of each group were aleatorily selected and following anesthesia, their heads severed; after histological treatment, serial 6 µm sections on the frontal plane at the molar level, stained with hematoxilin and eosin, were obtained. The experimental results produced, suggest that suckling from ethanol-treated mothers, show a significant decrease of body weight, significant alterations of karyometric and stereological measurements that determined hypotrophy of palatine epithelial cells and toxicity of ethanol at the palatine epithelium.

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“…Fetal alcohol syndrome (FAS), a phrase coined by Jones et al in 1973 (4, 5), describes the fetal consequence of maternal ethanol during pregnancy, and the associated array of physical dysmorphias, intrauterine growth retardation, and intellectual impairment postnatally (6)(7)(8)(9). The altered morphogenesis of the craniofacial region includes micropthalmia, midfacial and maxillary hypoplasia, cleft palate, poorly developed philtrums, thin upper lips, short noses, epicanthal folds, and microcephaly (4,(10)(11)(12)(13)(14)(15). Dysmorphogenesis of the limbs has also been observed (4,11,13) in addition to a variety of neural tube, cardiac and renal defects (11,12,14).…”

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Gestational exposure to ethanol suppresses msx2 expression in developing mouse embryos

Rifas

Towler

Avioli

1997

Proc. Natl. Acad. Sci. U.S.A.

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Ethanol acts as a teratogen in developing fetuses causing abnormalities of the brain, heart, craniofacial bones, and limb skeletal elements. To assess whether some teratogenic actions of ethanol might occur via dysregulation of msx2 expression, we examined msx2 expression in developing mouse embryos exposed to ethanol on embryonic day (E) 8 of gestation and subjected to whole mount in situ hybridization on E11-11.5 using a riboprobe for mouse msx2. Control mice exhibited expression of msx2 in developing brain, the developing limb buds and apical ectodermal ridge, the lateral and nasal processes, olfactory pit, palatal shelf of the maxilla, the eye, the lens of the eye, otic vesicle, prevertebral bodies (notochord), and endocardial cushion. Embryos exposed to ethanol in utero were significantly smaller than their normal counterparts and did not exhibit expression of msx2 in any structures. Similarly, msx2 expression, as determined by reverse transcription-PCR and Northern blot hybridization, was reduced Ϸ40-50% in fetal mouse calvarial osteoblastic cells exposed to 1% ethanol for 48 hr while alkaline phosphatase was increased by 2-fold and bone morphogenetic protein showed essentially no change. Transcriptional activity of the msx2 promoter was specifically suppressed by alcohol in MC3T3-E1 osteoblasts. Taken together, these data demonstrate that fetal alcohol exposure decreases msx2 expression, a known regulator of osteoblast and myoblast differentiation, and suggest that one of the ''putative'' mechanisms for fetal alcohol syndrome is the inhibition of msx2 expression during key developmental periods leading to developmental retardation, altered craniofacial morphogenesis, and cardiac defects.

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Renal anomalies in the fetal alcohol syndrome

Cited by 42 publications

References 5 publications

Effect of Intrauterine Ethanol Exposure on Fetal Lung Growth

Effect of Intrauterine Ethanol Exposure on Fetal Lung Growth

Histometric Study of the Epithelium of Rats Submitted to Ethanol During Lactation

Gestational exposure to ethanol suppresses msx2 expression in developing mouse embryos

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