The effects of trypan blue on the blood pressure of rat embryos.
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Abnormalities, Drug-Induced↗
Biomedical subjects
N Chernoff
Publications and source records attributed to N Chernoff.
Responses of the rat foetus to maternal injections of adrenaline and vasopressin.
1. Injection of 0.5-2.0 units of vasopressin or 25-100 mug of adrenaline into the peritoneal cavity of pregnant rats produced a transient slowing of the foetal heart. The bradycardia could be induced in foetuses after 15-21 days of gestation. Foetal heart rates dropped from normal values of 140-180 beats/min, often to less than 20 beats/minute. The period of bradycardia was dose dependent and ranged from 30 to 65 minutes.2. Maternal injection of the hormones produced a fall in foetal blood pressure from an average of 54, often to less than 20 mm of water, in 17-day foetuses. Direct injection of the hormones into the pericardial sac of the foetuses had the opposite effect and pressures rose an average of 15 mm of water 1 min after the injection.3. During the period of bradycardia, the potassium concentrations in foetal serum rose from an average value of 8.9 mequiv/1. to an average of 17.3 mequiv/litre. Concentrations of serum sodium fell from 126.2 to 121.4 mequiv/1. during the bradycardia. No changes were detected in the concentrations of either calcium or chloride. Foetal P(O2) levels fell from 25 to 15, P(CO2) rose from 61 to 89 or more, and pH fell from 7.19 to 6.86 during the bradycardia.4. Maternal death and uterine clamping caused foetal bradycardia and a rise in foetal serum potassium to an average of 20.2 mequiv/litre.5. It is concluded that interruption of normal uterine blood flow by vasoconstruction (adrenaline or vasopressin) or direct blockage (uterine clamping) results in a transient hypoxia, bradycardia, and serum ion changes in foetuses.
Animals↗
Supernumerary lumbar rib: manifestation of basic alteration in embryonic development of ribs.
Supernumerary ribs (SNR) are a common variant in some strains of mice used in standard teratology bioassays. We have previously demonstrated that increased incidence of SNR may be induced by a wide variety of xenobiotics and/or general maternal stress. The significance of this defect in cross-species extrapolations has been problematic and recent studies, including this one, have shown that this anomaly is more complex than previously thought. The SNR in mice have a bimodal distribution composed of 'rudimentary ribs' (RR) with a mode of 0.3-0.4 mm and 'extra ribs' (ER) with a mode of 0.9-1.1 mm. The studies reported here examine the relationship between the presence of SNR and the 13th rib length and the gross morphological development of the anomaly. Supernumerary ribs were induced in CD-1 mice by surgical stress (subcutaneous micropump implanted on gestational day (GD), restraint stress (GD8), food and water deprivation (GD8) or maternal administration of the pesticide dinoseb (50 mg kg-1 on GD7 and GD8). Fetuses from untreated litters were also examined. Dinoseb-treated mice were killed on GD14, 15, 16 or 17. All other groups were killed on GD17. The lengths of the 13th and 14th ribs were measured and other anomalies were recorded. Femur length was used as an indicator of fetal size. The SNR frequency was higher in all treatment groups compared to controls. We found that ER and RR were morphologically distinct. The ER were flat ended and distally joined by a cartilaginous portion, while RR were usually rounded distally and were without cartilaginous extensions. The 13th ribs were significantly longer in fetuses having SNR than in those not having SNR, whether treated or untreated. This relationship was present in all fetal ages examined and with both ER and RR groups. These results suggest that SNR are indicative of basic alterations in the development of the axial skeleton.
2,4-Dinitrophenol↗
Lack of teratogenicity of microcystin-LR in the mouse and toad.
Microcystin-LR (MC-LR) is a cyanobacterial toxin generated by the organism Microcystis aeruginosa. Although the hepatotoxicity of this chemical has been characterized, the potential developmental toxicity in vertebrates has not been well studied. The purpose of this study was to elucidate the effects of this toxin on the in vivo and in vitro development of mammals and the development of an Anuran (toad). Initial acute toxicity experiments with female CD-1 mice were accomplished with MC-LR administered i.p. in saline. Lethality occurred at 128 and 160 microg kg (-1) and histopathology revealed massive hepatic necrosis with diffuse hemorrhage. Developmental toxicity studies were done with MC-LR administered i.p. for 2-day periods: gestation days 7-8, 9-10 or 11-12. Doses used ranged from 2 to 128 microg kg(-1). On gestation day 17, fetuses were weighed and analyzed for gross morphological and skeletal defects. No treatment-related differences were seen in litter size, viability, weight or the incidence of anomalies. Groups of dams dosed with 32-128 microg kg(-1) on gestation days 7-8, 9-10 or 11-12 were allowed to give birth and the growth and development of their pups were followed postnatally. There were no significant effects noted in the offspring of the treated dams. Neurulation-staged CD-1 mouse conceptuses were exposed to 50-1000 nM MC-LR in whole embryo culture for 24 h. No significant increase in abnormalities or developmental delays was observed. Finally, exposure of the developing toad. Bufo arenarum was done from stage 17 (tail bud) for 10 days at concentrations of 1-20 mg l(-1). No effect on morphological development or survival was noted in any exposed groups. These data indicate that microcystin does not appear to affect development adversely in the mouse (in vivo or in vitro) or the toad at the doses and exposure parameters used.
Animals↗
An in vivo teratology screen utilizing pregnant mice.
Twenty-eight compounds of known teratogenic potential were assayed by an in vivo screening procedure. Postnatal growth and viability of prenatally exposed offspring was used as a measure of developmental toxicity. Gravid CD-1 mice were administered maximum tolerated doses of the compounds for up to 5 consecutive days during the period of major organogenesis. The dams were allowed to give birth, and litter size and weight on postpartum d 1 and 3 were recorded and compared with concurrent controls. All 15 compounds that were teratogenic by standard teratology test criteria exhibited some form of developmental toxicity. Four chemicals known to produce only fetal toxicity (reduced weight or supernumerary ribs) were tested and the screen successfully identified those that reduced weight. Finally, of the 9 compounds that show no effect in standard tests, 6 were also negative in the screen and 3 demonstrated either reduced viability or weight.
Abnormalities, Drug-Induced↗
Toxicity studies with decamethrin, a synthetic pyrethroid insecticide.
Decamethrin is a synthetic pyrethroid insecticide that has been under investigation by the World Health Organization for use in some vector control programs. Decamethrin proved to be a highly toxic pyrethroid ester. The acute LD50 for adult female rats was 31 mg/kg by the oral route and 4 mg/kg by the intravenous route of administration. The LD50 was observed to be sex and age dependent, with higher values recorded for weanlings and males. Initial signs of decamethrin poisoning include profuse salivation and convulsive movements. Weakness, dyspnea, anorexia and staining of the fur were observed beyond the first day following compound administration. Absorption of decamethrin was rapid by the inhalation route and minimal by the dermal route of administration. No evidence of teratogenic activity was found in rats or mice at dose levels that produced marked maternal toxicity, and no persistent toxicity was observed in neonatal rats that received perinatal exposure to decamethrin. No mutagenic activity was detected in three different in vitro assays, with or without metabolic activation.
Aerosols↗
Perinatal toxicity of endrin in rodents. I. Fetotoxic effects of prenatal exposure in hamsters.
The potential of the insecticide endrin to induce fetal toxicity was determined in hamsters exposed to the compound on either day 8 or days 5--14 of gestation. Endrin was administered by oral gavage as a solution in corn oil. Doses used included 0.5--10.0 mg/kg on day 8 and 0.75 to 3.5 mg/kg/day on days 5--14. Exposure to a single dose of endrin resulted in significant incidences of fused ribs and meningoencephaloceles at levels of 5 mg/kg or greater. No significant effects were noted in either maternal mortality and weight gain or in fetal mortality or weight gain. The administration of multiple doses of endrin resulted in few fetal defects, although a significant dose-related increase in fetal mortality and decrease in fetal weight was seen. Significant maternal lethality and weight reductions were noted at doses of 1.5 mg/kg/day or greater. At sacrifice, maternal liver and fetal tissues were collected and subsequently analyzed for endrin and a major metabolite, 12-ketoendrin. Endrin was found to cross the placenta and 20 ppb were found in fetuses from litters exposed to 2.5 mg/kg/day. Maternal livers from this dose group contained an average of 2500 pbb of endrin.
Abnormalities, Drug-Induced↗