[Effects of homocysteine on cardiovascular development in early chicken embryo].
OBJECTIVE
To study the relationship between homocysteine (HCY) and cardiovascular development in the early embryo and to determine whether folic acid and cobalamine (Vit B(12)) can reduce the developmental toxicity of HCY to cardiovascular system.


METHODS
Incubation test for chicken embryo, electron microscopy, methylgreen-pyronine stain, in situ fragment end labeling, and intervention trial with folic acid and vitamin B(12) were used in the study.


RESULTS
Treatment of 0 - 16.0 micromol of HCY/per embryo could disturb their heart development and differentiation of blood vessels at fetal ages of two and four days, in a dose-response pattern, with 24.1% and 25.0% of heart defect and 60.7% of inhibition of blood vessels of yolk sac in 8.0 micromol of HCY, respectively. A dose of more than four micromol/per embryo could damage the structure of myocardial cells and organelle, and inhibit the synthesis of cellular DNA and RNA. It was the first time to find that 8.0 micromol of HCY could induce excessive apoptosis of myocardial cells (2.7%), significantly higher than that in the normal control group. Folic acid could antagonize the cardiovascular toxicity caused by HCY, stronger than what Vit B(12) could do.


CONCLUSIONS
HCY was a new risk factor which could damage cardiovascular development, and folic acid could effectively antagonize its developmental toxicity. Cellular apoptosis might relate to cardiovascular defect.
Li
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Y
National Center for Maternal and Infant Health Care of China, Beijing Medical University, Beijing 100083.
Li
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Z
Chen
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Qi
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P
Li
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D000818:Animals; D002319:Cardiovascular System / Q000196:embryology; D002642:Chick Embryo; D005492:Folic Acid / Q000494:pharmacology*; D006330:Heart Defects, Congenital / Q000139:chemically induced*; D006710:Homocysteine / Q000037:antagonists & inhibitors / Q000633:toxicity*; D014805:Vitamin B 12 / Q000494:pharmacology*
D006710:Homocysteine; D005492:Folic Acid; D014805:Vitamin B 12