It has been hypothesized that homocysteine(HCY) can induce apoptosis at the organogenesis|stage of chick embryos and which can be the relationship between HCY and congenital defects of neural tube and heart.Exogenous D,L|HCY(4～8μmol/embryo) was injected into the place near brain and the yolk of the day 4 embryos.Then they were harvested 2 days later and examined by flow cytometry,histopathology,electronic microscope,in situ end labeling of DNA strand break and methylgreen|pyronine double staining.The change of plasma HCY level of day 10 embryos was also inspected by HPLC analysis.The HCY injected at different position of embryos could result in heart and neural tube defects,which included ectopia cardis,hydropericardium,endocardial cushion defect,encephalocele,microcephaly,abnormal flexions and so on.HCY could apparently disturb embryonic cell cycle,suppress the synthesis of DNA and RNA of embryonic cells.Excessive apoptotic cells in brain and heart were observed in HCY|treatment groups.It was discovered that mitochondrial damage could be described as an early event in cellular apoptosis of chick embryos.After 8 μmol of HCY was placed on the inner shell membrance,there was an obvious increase of plasma HCY concentration with a peak value of 80 58μmol/L in 120min,and followed by declining.On the other hand,5μg of folic acid given simultaneously with HCY could sharply curtail the rise in plasma HCY.It is concluded that HCY is a cytotoxin,inducing over apoptosis of embryos in some areas,which is coincident with the pathologic changes of neural system and heart.These findings show that there is a close relationship among HCY,apoptosis and birth defect in developing chick embryos.Mitochondrial dysmorphosis may be an important early event of apoptosis in embryos after exposure to HCY. It has been hypothesized that homocysteine ​​(HCY) can induce apoptosis at the organogenesis | stage of chick embryos and which can be the relationship between HCY and congenital defects of neural tube and heart. Exogenous D, L | HCY (4 ~ 8 μmol / embryo) was injected into the place near brain and the yolk of the day 4 embryos. They were harvested 2 days later and examined by flow cytometry, histopathology, electronic microscope, in situ end labeling of DNA strand break and methylgreen | pyronine double staining. change of plasma HCY level of day 10 embryos was also inspected by HPLC analysis. HCY injected at different position of embryos could result in heart and neural tube defects, which include ectopia cardis, hydropericardium, endocardial cushion defect, encephalocele, microcephaly, abnormal flexions and so on. HCY could apparently disturb embryonic cell cycle, suppress the synthesis of DNA and RNA of embryonic cells. Excess apoptotic cells in brain and heart were observed in HCY | trea tment groups. It was discovered that mitochondrial damage could be described as an early event in cellular apoptosis of chick embryos. After 8 μmol of HCY was placed on the inner shell membrance, there was an obvious increase of plasma HCY concentration with a peak value of 80 58 μmol / L in 120 min, followed by declining. Of the other hand, 5 μg of folic acid given simultaneously with HCY could sharply curtail the rise in plasma HCY. It is said that HCY is a cytotoxin, inducing over apoptosis of embryos in some areas, which is coincident with the pathologic changes of neural system and heart. these findings show that there is a close relationship among HCY, apoptosis and birth defects in developing chick embryos. Mitochondrial dysmorphosis may be an important early event of apoptosis in embryos after exposure to HCY.