Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] · 1999
[Effects of homocysteine on cardiovascular development in early chicken embryo].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Y, Li Z, Chen X, Qi P, Li S
Аннотация
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.
CONCLUSION: 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.
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.
CONCLUSION: 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.