Suppr超能文献

产前乙醇暴露会扰乱胎儿骨骼发育的组织学阶段。

Prenatal ethanol exposure disrupts the histological stages of fetal bone development.

作者信息

Snow M E, Keiver K

机构信息

Food, Nutrition and Health, Faculty of Land and Food Systems, The University of British Columbia, Vancouver, Canada.

出版信息

Bone. 2007 Aug;41(2):181-7. doi: 10.1016/j.bone.2007.04.182. Epub 2007 Apr 25.

Abstract

Maternal ethanol intake during pregnancy results in impairments in general growth and skeletal development in the offspring. We have previously shown that ethanol retards skeletal ossification at doses lower than those that affect growth. Moreover, skeletal sites vary in their sensitivity to ethanol effects, with more severe effects occurring in bones that undergo a greater proportion of their development in utero. Taken together, these data suggest that ethanol has specific effects on bone development, and that later stages in the ossification process may be particularly affected. Such effects could have important implications for the offspring's long-term bone health, as studies suggest that the intrauterine environment can program the skeleton. The present study examined the histological stages of bone development to determine if prenatal ethanol exposure alters the morphological development of the growth plate in the fetal rat. Rats were fed a liquid diet containing ethanol (Ethanol, E group), or without ethanol (Pair-Fed, PF, or Control, C groups) for 6 weeks: 3 weeks prior to breeding and during 3 weeks of pregnancy. Fetal tibiae were fixed, decalcified and stained for histological analysis on day 21 of gestation. Maternal ethanol intake resulted in a significant decrease in fetal total bone and diaphysis lengths, compared with tibiae from PF and C fetuses. Although the lengths of the epiphyses were not affected, ethanol disrupted the organization of the histological zones within the epiphyses. Prenatal ethanol exposure decreased the length of the resting zone, but increased the length of the hypertrophic zone. Enlargement of the hypertrophic zone is consistent with an effect of ethanol on the later stages of bone development; however, ethanol's effect on the resting zone indicates that earlier stages of bone development may also be disrupted. The functional significance of these morphological changes to long-term bone health remains to be determined.

摘要

孕期母体摄入乙醇会导致后代总体生长和骨骼发育受损。我们之前已经表明,乙醇在低于影响生长剂量的情况下会延缓骨骼骨化。此外,骨骼部位对乙醇作用的敏感性各不相同,在子宫内发育比例较大的骨骼受到的影响更为严重。综合来看,这些数据表明乙醇对骨骼发育有特定影响,并且骨化过程的后期阶段可能受到特别影响。此类影响可能对后代的长期骨骼健康具有重要意义,因为研究表明子宫内环境可对骨骼产生编程作用。本研究检查了骨骼发育的组织学阶段,以确定产前乙醇暴露是否会改变胎鼠生长板的形态发育。大鼠在配种前3周及孕期3周期间喂食含乙醇的液体饲料(乙醇组,E组)或不含乙醇的液体饲料(配对喂食组,PF组,或对照组,C组),为期6周。在妊娠第21天对胎儿胫骨进行固定、脱钙并染色以进行组织学分析。与PF组和C组胎儿的胫骨相比,母体摄入乙醇导致胎儿总骨长度和骨干长度显著降低。虽然骨骺长度未受影响,但乙醇破坏了骨骺内组织学区域的组织结构。产前乙醇暴露缩短了静止区长度,但增加了肥大区长度。肥大区增大与乙醇对骨骼发育后期阶段的影响一致;然而乙醇对静止区的影响表明骨骼发育的早期阶段也可能受到破坏。这些形态学变化对长期骨骼健康的功能意义仍有待确定。

相似文献

1
Prenatal ethanol exposure disrupts the histological stages of fetal bone development.
Bone. 2007 Aug;41(2):181-7. doi: 10.1016/j.bone.2007.04.182. Epub 2007 Apr 25.
2
3
Effect of duration of maternal alcohol consumption on calcium metabolism and bone in the fetal rat.
Alcohol Clin Exp Res. 2004 Mar;28(3):456-67. doi: 10.1097/01.alc.0000118312.38204.c5.
4
Effect of prenatal ethanol exposure on fetal calcium metabolism.
Alcohol Clin Exp Res. 1997 Dec;21(9):1612-8.
6
Alterations of maternal estrogen levels during gestation affect the skeleton of female offspring.
Endocrinology. 1996 May;137(5):2118-25. doi: 10.1210/endo.137.5.8612556.
7
Fetal ethanol effects on benzodiazepine sensitivity measured by behavior on the elevated plus-maze.
Pharmacol Biochem Behav. 1998 Jul;60(3):625-33. doi: 10.1016/s0091-3057(98)00039-2.
8
Effect of 6 GHz radiofrequency electromagnetic field on the development of fetal bones.
Electromagn Biol Med. 2025 Jan 2;44(1):17-25. doi: 10.1080/15368378.2024.2438608. Epub 2024 Dec 18.
9
Effect of maternal ethanol consumption on maternal and fetal calcium metabolism.
Alcohol Clin Exp Res. 1996 Oct;20(7):1305-12. doi: 10.1111/j.1530-0277.1996.tb01127.x.
10
Skeletal toxicity associated with chronic ethanol exposure in a rat model using total enteral nutrition.
J Pharmacol Exp Ther. 2002 Jun;301(3):1132-8. doi: 10.1124/jpet.301.3.1132.

引用本文的文献

1
Astrocyte Extracellular Matrix Modulates Neuronal Dendritic Development.
Glia. 2025 Aug;73(8):1589-1607. doi: 10.1002/glia.70020. Epub 2025 Apr 7.
2
Astrocyte extracellular matrix modulates neuronal dendritic development.
bioRxiv. 2024 Aug 22:2024.08.06.606424. doi: 10.1101/2024.08.06.606424.
3
Sexually dimorphic effects of prenatal alcohol exposure on the murine skeleton.
Biol Sex Differ. 2024 Jun 18;15(1):51. doi: 10.1186/s13293-024-00626-y.
6
Extracellular Vesicles in Premature Aging and Diseases in Adulthood Due to Developmental Exposures.
Aging Dis. 2021 Sep 1;12(6):1516-1535. doi: 10.14336/AD.2021.0322. eCollection 2021 Sep.
8
Ethanol Alters Phenotype and Synthesis Activity of Rat Neonatal Articular Chondrocytes Grown in 2- and 3-Dimensional Culture.
Cartilage. 2021 Dec;13(2_suppl):839S-846S. doi: 10.1177/1947603519870862. Epub 2019 Aug 23.
9
The role of acidemia in maternal binge alcohol-induced alterations in fetal bone functional properties.
Alcohol Clin Exp Res. 2013 Sep;37(9):1476-82. doi: 10.1111/acer.12118. Epub 2013 May 3.
10
Commonality in Down and fetal alcohol syndromes.
Birth Defects Res A Clin Mol Teratol. 2013 Apr;97(4):187-97. doi: 10.1002/bdra.23129. Epub 2013 Apr 3.

本文引用的文献

1
Intraclass correlations: uses in assessing rater reliability.
Psychol Bull. 1979 Mar;86(2):420-8. doi: 10.1037//0033-2909.86.2.420.
2
Binge alcohol exposure during all three trimesters alters bone strength and growth in fetal sheep.
Alcohol. 2006 Apr;38(3):185-92. doi: 10.1016/j.alcohol.2006.06.004. Epub 2006 Jul 26.
3
Prenatal alcohol exposure and fetal programming: effects on neuroendocrine and immune function.
Exp Biol Med (Maywood). 2005 Jun;230(6):376-88. doi: 10.1177/15353702-0323006-05.
4
5
Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis.
CMAJ. 2005 Mar 1;172(5 Suppl):S1-S21. doi: 10.1503/cmaj.1040302.
6
Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.
Development. 2004 Dec;131(23):5883-95. doi: 10.1242/dev.01461.
7
Adipogenic effect of alcohol on human bone marrow-derived mesenchymal stem cells.
Alcohol Clin Exp Res. 2004 Jul;28(7):1091-101. doi: 10.1097/01.alc.0000130808.49262.f5.
8
Inhibitory effect of alcohol on osteogenic differentiation in human bone marrow-derived mesenchymal stem cells.
Alcohol Clin Exp Res. 2004 Mar;28(3):468-79. doi: 10.1097/01.alc.0000118315.58404.c1.
9
Effect of duration of maternal alcohol consumption on calcium metabolism and bone in the fetal rat.
Alcohol Clin Exp Res. 2004 Mar;28(3):456-67. doi: 10.1097/01.alc.0000118312.38204.c5.
10
VEGFA is necessary for chondrocyte survival during bone development.
Development. 2004 May;131(9):2161-71. doi: 10.1242/dev.01053. Epub 2004 Apr 8.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验