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The embryotoxicity of gentamicin was evaluated with rat whole embryo culture (WEC) assay. Rat embryos displaying 1-3 somites were explanted on gestation day (GD) 9.5 and cultured for 48 h in rat serum. Gentamicin sulfate was added to the culture medium at a concentration of 1, 10 and 100 μg/ml. At the end of the cultivation five endpoints were evaluated for each viable embryo: yolk-sac diameter, crown-rump length, head length, somites number and morphological score. Gentamicin at the concentration of 100 μg/ml was embryotoxic and caused growth retardation in rat embryos. At the concentration of 10 μg/ml about 45% of embryos showed haematomas. The lowest dose of antibiotic (1 μg/ml) did not interfere with embryonic development in vitro.
Administration of the Ascaris tegumental homogenate (0.6-1.2 g of Ascaris proteins/kg/day) at a early stage of organogenesis (5-9 days of pregnancy) had a harmful effect upon the developing mouse fetuses. It has been found that injection of the homogenate did not delay or prevent implantation, but causes a high rate of intrauterine deaths. The Ascaris homogenate significantly decreased the number of live fetuses per litter, increased the frequency of litter resorption, produced a delay in bone formation and induced pathological changes of fetal organs and tissues. The congenital malformations were noted in fetuses after injection of higher doses of Ascaris homogenate (exencephaly, craniomeningocele and intemal hydrocephalus). No malformations were noted in control groups and after injection of minimum dose of the homogenate. The symptoms that occurred after administration of the tegumental homogenate to pregnant mice included: decreased body weight gain (p<0.001) as compared to controls, vaginal hemorrhage, intrauterine resorption of litter and mortality. These signs suggest that the Ascaris homogenate causes matemal toxicity.
Administration intraperitoneally of the Ascaris suum extract - ASE-(0.6-1.4 g of Ascaris proteins/kg/day) at a late stage of organogenesis (8-12 days of gestation) disturbed course of mouse pregnancy. lt has been found that injections of higher doses of ASE to pregnant mice caused the symptoms manifesting maternal toxicity (decreased body weight gain /p < 0.001/ as compared to control, intrauterine resorption of litter, vaginal hemorrhages, female mortality and altered behaviour). There is a linear interrelationship between the logarithm of the dose of ASE and mortality of pregnant mice. The DL₅₀ value of Ascaris proteins for pregnant mice was 1.02 g/kg/day (confidence interval 0.97-1.07 g/kg/day). ASE exerted embryotoxic effects: significantly decreased the number of surviving fetuses per litter and the mean body weight of fetuses, increased the number of fetal resorptions.
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