摘要
One hundred and ninety-five mice were used to study the mechanism of the protective ef-fects of folic acid on nitroqine toxicity to the small intestine.After oral administration of nitroquineacetate(570mg/kg×1),intramuscular injection of normal saline was given to one group of mice(NS group)and intramuscular injection of folic acid(8mg/kg×1)to another(NF group).Decrease incells in the crypts were observed in the animals of NS group,but the changes were much milder inthose of NF group even at 96 h after administration.The decrease of DNA content in the tissues ofthe small intestine was dose-and time-dependent.The value of cpm/mg of DNA after ~3H-TdRincorporation were much higher in NF group than in NS group.these rcsults suggest that DNA synthesis in the small intestine may be promoted by folic acid so thatthe renair of the damaged intestinal mucosa is acoelerated.
One hundred and ninety-five mice were used to study the mechanism of the protective ef- fects of folic acid on nitroqine toxicity to the small intestine.After oral administration of nitroquine acetate(570mg/kg×1),intramuscular injection of normal saline was given to one group of mice(N S group)and intramuscular injection of folic acid(8mg/kg×1)to another(NF group).Decrease in cells in the crypts were observed in the animals of NS group,but the changes were much milder in those of NF group even at 96 h after administration.The decrease of DNA content in the tissues of the small intestine was dose-and time-dependent.The value of cpm/mg of DNA after ~3H-TdR incorporation were much higher in NF group than in NS group. these rcsults suggest that DNA synthesis in the small intestine may be promoted by folic acid so that the renair of the damaged intestinal mucosa is acoelerated.
