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Effect of a single dose of ethanol on developing skeletal muscle of chick embryos
1Department of Anatomy, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110029, India. joydeep@canada.com
Insights
Ethanol exposure during pregnancy causes fetal alcohol syndrome (FAS), leading to growth retardation. This study found ethanol directly damages skeletal muscle in chick embryos, explaining growth deficits in FAS.
Area of Science:
- Developmental Biology
- Toxicology
- Embryology
Background:
- Fetal alcohol syndrome (FAS) is linked to postnatal growth retardation in children, even with adequate nutrition.
- Animal studies suggest allometric skeletal muscle growth retardation contributes to FAS growth deficits.
- The precise mechanisms behind ethanol-induced skeletal muscle growth impairment in FAS remain unclear.
Purpose of the Study:
- To investigate structural changes in skeletal muscle of chick embryos exposed to ethanol.
- To elucidate the mechanisms of growth retardation associated with fetal alcohol syndrome.
Main Methods:
- Chick embryos were exposed to varying doses of ethanol (5%, 10%, 15%).
- General growth parameters (crown rump length, head circumference, body weight) were measured.
- Skeletal muscle weight and microscopic structure were analyzed.
Main Results:
- Ethanol exposure significantly retarded embryo growth (crown rump length, head circumference, body weight).
- Skeletal muscle weights were proportionally reduced in ethanol-exposed chicks.
- Microscopic analysis revealed neutrophil infiltration and necrosis in skeletal muscle at higher ethanol doses (10%, 15%).
Conclusions:
- A single ethanol dose has direct toxic effects on developing chick embryos, particularly skeletal muscle.
- Ethanol-induced skeletal muscle damage in embryos may explain postnatal growth failure observed in fetal alcohol syndrome.
Abstract:
Fetal alcohol syndrome is a condition occurring in some children of mothers who have consumed alcohol during pregnancy. Many of these affected children show retarded physical growth in the postnatal period despite adequate nutrition. On the basis of findings from studies with animals, it has been proposed that this is due to allometric retardation of growth of skeletal muscle, although the exact reasons for this are not known. The aim of the current study was to examine the structural changes in skeletal muscle in fetal alcohol syndrome in an attempt to understand the mechanisms of growth retardation in fetal alcohol syndrome. Chick embryos were exposed to single doses of 5%, 10%, and 15% ethanol, and the effects on the general growth and development, as well as on the skeletal muscle, of these chicks were studied. There was a significant retardation in crown rump length, head circumference, and body weight in ethanol-exposed chicks when these parameters were compared with findings for appropriate control groups. This retardation was associated with significant and proportionate reductions in the weights of skeletal muscles. Microscopic examination of skeletal muscle showed areas of neutrophil infiltration and necrosis, suggestive of muscle damage, in chicks exposed to 10% and 15% ethanol. Thus, findings of the current study demonstrate the direct toxic effects of a single dose of ethanol on developing embryos in general and skeletal muscle in particular. The pathologic changes seen in skeletal muscle could account for the failure in postnatal growth in fetal alcohol syndrome.
