ABSTRACT
Trypsin inhibitor isolated from Ascaris suum and injected into pregnant BALB/c mice (five times, in doses: 300 or 400 mg/kg/day) in various periods of pregnancy (early and late organogenesis) disturbed the development of fetuses. The nature and intensity of prenatal disturbances are determined by the inhibitor dose and time of injection. It has been found that administration of the inhibitor from 5-th until 9-th day of gestation did not delay or prevent implantation, but caused a high rate of intrauterine deaths and also specific congenital malformations (exnencephaly and hydrocephalus). Additionally, other types of defects were noted in fetuses after injection of the inhibitor between 8-th and 12-th day of pregnancy (cleft palate, fusion of ribs). Independent of the time of injection during gestation the inhibitor exhibited embriotoxic effects (e.g. decreased the number of live fetuses per litter and mean fetal weight).
Subject(s)
Abnormalities, Drug-Induced/parasitology , Helminth Proteins/toxicity , Pregnancy Complications, Parasitic/chemically induced , Prenatal Exposure Delayed Effects , Teratogens/toxicity , Animals , Dose-Response Relationship, Drug , Female , Fetal Death/chemically induced , Fetal Weight/drug effects , Gestational Age , Litter Size/drug effects , Maternal-Fetal Exchange/drug effects , Mice , Mice, Inbred BALB C , Organogenesis/drug effects , PregnancyABSTRACT
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 internal 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 maternal toxicity.
Subject(s)
Abnormalities, Drug-Induced/parasitology , Helminth Proteins/toxicity , Pregnancy Complications, Parasitic , Prenatal Exposure Delayed Effects , Teratogens/toxicity , Animals , Ascaris , Body Weight/drug effects , Dose-Response Relationship, Drug , Endpoint Determination/methods , Female , Fetal Death/chemically induced , Fetal Resorption/chemically induced , Fetal Weight/drug effects , Litter Size/drug effects , Maternal-Fetal Exchange/drug effects , Mice , Mice, Inbred BALB C , Organogenesis/drug effects , Pregnancy , Toxicity TestsABSTRACT
Para avaliar a açäo do albendazol sobre larvas de terceiro estágio de Lagochilascaris minor foram empregados 60 camundongos isogênicos C57BL/6, divideos em três grupos iguais. Cada animal foi inoculado com 10ü ovos infectantes de L. minor, via oral, através de uma sonda esofagiana. Todos os animais dos Grupos I e II foram tratados individualmente com albendazol, na dosagem de 400 mg/Kg/dia, via oral, durante 30 dias. Tendo em vista o padräo de migraçäo de larvas de L. minor no organismo de camundongo (hospedeiro intermediário), os animais do Grupo I receberam a droga a partir do 7º dia e os do Grupo II, no 60º dia após o término do uso da droga, todos os animais de cada grupo foram necropsiados. O número de larvas vivas recuperadas dos nódulos da musculatura esquelética do tecido celular subcutâneo e das vísceras foi o critério utilizado para avaliar a eficácia da droga. Foram observados níveis de eficácia de 80,9(pôr cento) para o Grupo I e de 66,3 (pôr cento) para o Grupo II. Podemos inferir que ambos os esquemas terapêuticos utilizados neste trabalho foram ineficazes no tratamento da lagochilascaríase murina experimental
