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Biomedical subjects

C J Price

Publications and source records attributed to C J Price.

125 records · Page 7Linked to original sources
PubMed1986

The developmental toxicity of orally administered oxytetracycline in rats and mice.

Timed-pregnant CD rats and CD-1 mice were dosed by gavage with oxytetracycline hydrochloride (OXT) in corn oil on gestational days (gd) 6-15 (0, 1200, 1350, or 1500 mg/kg/day for rats; 0, 1325, 1670, or 2100 mg/kg/day for mice). Deaths among treated females occurred in a dose-related manner in all OXT dose groups (2-7%, mice; 5-24%, rats), but no maternal deaths occurred in the vehicle control groups. Significant dose-related decreases in maternal weight gain during treatment, as well as for corrected gestational weight gain (i.e., maternal gestational weight gain minus gravid uterine weight), were observed at all doses in rats but not in mice. Gravid uterine weight was reduced in a dose-related manner only in mice, with the high-dose group significantly reduced compared to the control group. At termination (gd 20, rats; gd 17, mice), the status of uterine implantation sites was recorded and live fetuses were weighed. Fetuses were examined for external, visceral, and skeletal abnormalities. There were no significant effects of OXT in either species on the incidence of postimplantation loss (resorptions plus dead fetuses) or malformations. In both species, there was a significant trend toward reduced fetal body weight, and each group of rats receiving OXT was significantly reduced compared to the control group. Administration of OXT during organogenesis at doses exceeding the therapeutic range for humans produced maternal and fetal toxicity, but did not produce any treatment-related increase in malformations.

Animals↗
PubMed1985

Teratologic and postnatal evaluation of aniline hydrochloride in the Fischer 344 rat.

Timed-pregnant Fischer 344 rats were dosed by gavage with aniline hydrochloride (10, 30, or 100 mg/kg/day), a positive control agent (hydroxyurea, 200 mg/kg/day), or vehicle (distilled water) on gestational days (gd) 7 through 20 or gd 7 through parturition. At termination on gd 20 confirmed-pregnant dams exhibited characteristic signs of aniline HCl toxicity, i.e., methemoglobinemia, increased relative spleen weight, decreased red blood cell (RBC) count, and hematological changes indicative of increased hematopoietic activity. High-dose dams exhibited mild methemoglobinemia, increased relative spleen weight, and increased RBC size at termination on postnatal day (pnd) 30. At termination on gd 20, fetuses from aniline-treated dams exhibited increased relative liver weight and enhanced hematopoietic activity, but no evidence of an embryolethal or teratogenic effect was observed. Postnatal signs of toxicity in litters from aniline-treated dams (i.e., decreased body weight, elevated relative liver weight, and elevated relative spleen weight) were transient, and no evidence of toxicity was observed in pups surviving to pnd 60. Hydroxyurea (200 mg/kg/day) administered by gavage proved to be an excellent positive control for embryotoxicity, maternal toxicity, teratogenicity, and postnatal maturational deficits in the Fischer 344 rat. In conclusion, aniline hydrochloride was not teratogenic to Fischer 344 rats, even at maternally toxic doses; transient signs of toxicity were observed postnatally in the offspring in conjunction with mild, but persistent signs of maternal toxicity through pnd 30.

Abnormalities, Drug-Induced↗
PubMed1985

The developmental toxicity of ethylene glycol in rats and mice.

Timed-pregnant CD rats and CD-1 mice were dosed by gavage with ethylene glycol (EG) in distilled water on gestational days (gd) 6 through 15 (0, 1250, 2500, or 5000 mg kg-1 day-1 for rats; and 0, 750, 1500, or 3000 mg kg-1 day-1 for mice). Females were observed daily during treatment, but no maternal deaths or distinctive clinical signs were noted. Dose-related decreases in maternal weight gain during treatment were significant at all doses in rats and at the mid and high doses in mice. Gravid uterine weight was reduced in both species at the mid and high doses, and corrected maternal gestational weight gain showed a significant decreasing trend. At termination (gd 20, rats; gd 17, mice), the status of uterine implantation sites was recorded, and live fetuses were weighed and examined for external, visceral, and skeletal malformations. Dose-related increases in postimplantation loss per litter were observed in both species with the high dose significantly above controls only in rats. Fetal body weight per litter was significantly reduced at the mid and high doses in rats and at all doses in mice. The percentage of malformed live fetuses per litter and/or the percentage of litters with malformed fetuses was significantly elevated in all EG dose groups and greater than 95% of litters were affected at the high dose for each species. A wide variety of malformations were observed; the most common in both species were craniofacial and neural tube closure defects and axial skeletal dysplasia. EG produced severe developmental toxicity in two rodent species at doses that apparently failed to produce any serious maternal effects.

Animals↗
PubMed1985

Teratologic evaluation of dinitrotoluene in the Fischer 344 rat.

Technical grade dinitrotoluene (DNT) was administered by gavage (po) to timed-pregnant Fischer 344 rats on Gestational Days (gd) 7 through 20. Mortality rates for the DNT (14, 35, 37.5, 75, 100, or 150 mg/kg/day) groups were 4.5, 7.7, 0.0, 0.0, 4.3, and 46.2% of treated females, respectively. No deaths occurred in the positive control (hydroxyurea, 200 mg/kg/day) or vehicle control (corn oil) groups. At sacrifice on gd 20, the hematological profile for dams in the 100-mg/kg/day group exhibited characteristic signs of DNT toxicity. Treatment-related increases in maternal relative liver and spleen weight (% body weight), and a dose-related decrease in absolute maternal weight gain during gestation (i.e., minus gravid uterine weight) were observed across all DNT groups. A notable increase in prenatal mortality occurred at the high dose (16.8% resorptions or late fetal deaths per litter for controls vs 49.6% for DNT), but but did not reach statistical significance. No statistically significant effects on fetal growth or morphological development as a result of DNT treatment were observed. Hydroxyurea produced mild hematoxicity in dams and fetuses. Effects of hydroxyurea on fetal growth and morphological development included decreased fetal body weight and crown-rump length, and an increased percentage of malformed fetuses (30% per litter). In conclusion, DNT was not found to be teratogenic following oral administration to Fischer 344 rats; embryo/fetal toxicity was observed only at a dose which also produced 46.2% maternal mortality.

Animals↗
PubMed1972

Stimulation of the production of unesterified fatty acids in nerve endings of guinea-pig brain in vitro by noradrenaline and 5-hydroxytryptamine.

1. Noradrenaline (1mm) and 5-hydroxytryptamine (1mm) stimulated the production of unesterified palmitate, oleate, stearate and arachidonate in nerve endings (synaptosomes) isolated from combined guinea-pig cerebral cortex and cerebellum. 2. Iproniazid phosphate (0.36mm) increased the concentrations of the same acids in osmotically ruptured synaptosomes. Further addition of 1mm-noradrenaline or 1mm-5-hydroxytryptamine reversed this increase. 3. Noradrenaline (0.01mm) stimulated the production of unesterified fatty acids in isolated synaptic membranes. 5-Hydroxytryptamine (0.01mm) stimulated the production of unesterified fatty acids in synaptic membranes and synaptic vesicles.

Animals↗
PubMedDate not supplied

Developmental toxicity evaluation of 1,2,3,4-butanetetracarboxylic acid in Sprague Dawley (CD) rats.

1,2,3,4-butanetetracarboxylic acid (BTCA), proposed as a formaldehyde substitute in the treatment of permanent press fabrics, was evaluated for developmental toxicity. Timed-mated CD rats (25 per group) received BTCA 250, 500, or 1000 mg/kg/day or vehicle (deionized/distilled water) by gavage on gestational days (gd) 6 through 19. Maternal feed and water consumption, body weight, and clinical signs were monitored throughout gestation. At termination (gd 20), confirmed-pregnant females (21 to 25 per group) were evaluated for clinical status and gestational outcome; live fetuses were examined for external, visceral, and skeletal malformations. One maternal death, reduced body weight, and reduced weight gain were noted at the high dose; confirmed pregnancy rates were 84 to 100% for each group. There were no treatment-related effects on fetal growth, survival, or morphologic development. The maternal toxicity NOAEL and LOAEL are 500 and 1000 mg/kg/day, respectively. The developmental toxicity NOAEL is > or = 1000 mg/kg/day, and the LOAEL was not established in this study.

Administration, Oral↗
PubMedDate not supplied

Blood boron concentrations in pregnant rats fed boric acid throughout gestation.

Timed-mated Sprague-Dawley rats (28 to 32/group) were exposed to boric acid (BA) in the diet from Gestational Day (GD) 0 to 20. Dietary concentrations of added BA (0%, 0.025%, 0.050%, 0.075%, 0.100%, or 0.200%) yielded average daily intakes equivalent to 0, 3, 6, 10, 13, or 25 mg boron/kg body weight/d. Dams and their fetuses were evaluated for evidence of maternal or developmental toxicity, as reported previously. At termination on GD 20, maternal whole blood was collected in heparinized Vacutainer tubes, stored frozen (-20 degrees C), and subsequently prepared by a high-temperature alkaline ashing procedure for analysis of boron by inductively coupled plasma optical emission spectrometry. Increasing dietary concentrations of BA were positively associated with whole blood boron concentrations in confirmed pregnant rats, specifically 0.229 +/- 0.143, 0.564 +/- 0.211, 0.975 +/- 0.261, 1.27 +/- 0.298, 1.53 +/- 0.546, or 2.82 +/- 0.987 micrograms boron/g whole blood (mean +/- SD) for the control through high-dose groups. Maternal blood boron concentrations were positively correlated with indices of maternal dietary intake of boron and with embryo/fetal toxicity observed at 0.100% and 0.200% BA in the diet reported previously. Thus, blood boron concentrations of 1.27 +/- 0.298 and 1.53 +/- 0.546 micrograms boron/g were associated with the no-observed-adverse-effect level (10 mg boron/kg/d) and lowest-observed-adverse-effect level (13 mg boron/kg/d) for developmental toxicity reported previously.

Animals↗
PubMedDate not supplied

General, reproductive, developmental, and endocrine toxicity of boronated compounds.

Boric acid and inorganic borates are abundant in nature. They are widely used in industrial, agricultural, cosmetic, and numerous smaller applications. These compounds are toxic to all species tested at high doses, but they are not carcinogenic or mutagenic. The major toxicities are reproductive and developmental. Testicular effects occurred at approximately 26 mg boron equivalents/kg body weight (bw)/d (26 mg boron equivalent (BE)/kg bw/d). New data on endocrine toxicity includes altered follicle stimulating hormone and testosterone within 14 d of treatment. Because these hormonal changes may be secondary effects of testicular toxicity, borates are not suspect as endocrine disrupters. The most sensitive of all the endpoints are prenatal growth and morphologic development in the rat; these changes occurred at a dose of 12.9 mg BE/kg bw/d. The no observed adverse effect level for rat fetal development was 9.6 mg/kg BE. Considering the estimated human exposure levels and a safety factor of 30, humans are not at significant risk of reproductive failure due to borates from environmental sources. The margin of exposure is estimated at 72 for males and 129 for females. Thus, the likelihood of human toxicity caused by boric acid and inorganic borates from exposure during normal activities is remote.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Effects of low-level carbon monoxide exposure on resting and exercise-induced ventricular arrhythmias in patients with coronary artery disease and no baseline ectopy.

The effects of acute elevation of carboxyhemoglobin (COHb) concentrations on resting and exercise-induced ventricular arrhythmias were evaluated in 10 patients who had ischemic heart disease and in whom no ectopy during baseline monitoring was noted. After an initial training session, patients were exposed to air, 100 ppm carbon monoxide (CO), or 200 ppm CO on successive days in a randomized, double-blind, cross-over fashion. After exposure to 100 and 200 ppm CO, venous COHb levels averaged 4% and 6%, respectively. Symptom-limited supine exercise was performed after exposure. Eight of the 10 patients had evidence of exercise-induced ischemia--either angina, 1.0 mm ST depression, or abnormal ejection fraction response--during 1 or more exposure days. Ambulatory electrocardiograms were obtained on each day and analyzed for arrhythmia frequency and severity. On air and CO exposure days, each patient had only 0-1 ventricular premature beat/h in the 2 h prior to exposure, during the exposure period, during the subsequent exercise test, and in the 5 h following exercise. In conclusion, low-level CO exposure is not arrhythmogenic in patients with coronary artery disease and no ventricular ectopy at baseline.

Aged↗
PubMedDate not supplied

Demonstrating the implicit processing of visually presented words and pseudowords.

This study demonstrates that even when subjects are instructed to perform a nonlinguistic visual feature detection task, the mere presence of words or pseudowords in the visual field activates a widespread neuronal network that is congruent with classical language areas. The implication of this result is that subjects will process words beyond the functional demands of the task. Therefore, contrasting brain activity in a word task that explicitly requires a cognitive function with a word task in which the function is activated implicitly will not necessarily isolate the brain area of interest. Furthermore, in most brain regions, we found that pseudowords, which have unfamiliar phonological associations and no associated semantic association, produce greater activation than words. Greater brain activity associated with pseudowords illustrates that unfamiliar stimuli that are unable to access word associations may activate the neuronal network more strongly than familiar words for which access occurs with ease.

Brain↗