Search PubMed⌕ Search

Biomedical subjects

J K Haseman

Publications and source records attributed to J K Haseman.

At least 163 records · Page 9Linked to original sources
PubMed1976

The transmission of reflexes in the spinal cord of cats during direct irradiation with microwaves.

The spinal of cats was directly exposed to 2450 CW microwave radiation in order to study the effect on reflex response and synaptic function. A small but statistically significant increase in the reflex response was detected in the first series of experiment, which indicates enhancement of the synaptic transmission. However, this effect was not observed in a second series of experiments in which the incident power density was increased from 10 mW/cm(2) to 20 mW/cm(2) and a more rigorous experimental design was employed. The slight changes that were observed in the second series could be attributed to small temperature variations during the experiment.

Animals↗
PubMed1976

Developmental toxicity in the rat after ingestion or gavage of organophosphate pesticides (Dipterex, Imidan) during pregnancy.

The structural development of fetuses was altered when Dipterex was administered by diet to pregnant rats from days 6 through 15 of gestation. Major external and skeletal alterations occurred after consumption of 432 or 519 mg/kg body weight per day, only minor skeletal changes occurred in the 375 mg/kg dose group and the incidence of alterations in the 145 mg/kg dose group was not significantly different from that in the pair-fed controls. The malformations seen at the two highest doses did not result directly from the associated decrease in food consumed. Dipterex was not shown to have teratogenic potential when given for the same time span, once daily by gavage, even at levels that produced maternal lethality. Imidan was not teratogenic when similarly given, either by diet at concentrations that resulted in a 45% reduction in food consumption, or by gavage at dose levels that resulted in some maternal lethality. Data collected from pair-fed control females revealed that limitation of food consumption to 13--15 g/rat per day from days 6 through 15 of gestation did not result in increased fetal mortality or stunting. However, fetal weight was reduced slightly, and the incidence of minor skeletal changes was approximately three to four times that among fetuses of control dams that were not pair-fed.

Abnormalities, Drug-Induced↗
PubMed1975

Selection of the experimental unit in teratology studies.

In teratology experiments the litter (pregnant female) rather than the fetus is advocated as being the proper experimental unit upon which to base the statistical analysis. It is pointed out that per litter tests, by being based on the average fetal response within a litter, do take the individual fetus into account. Actual experimental data are used to show that when litter effects are present a per fetus analysis is invalid and may seriously exaggerate the significance level. It is also shown that there appears to be little loss in sensitivity in performing per litter tests even in the unlikely event that there are no litter effects. Thus it certainly seems prudent to analyze teratology data with test procedures that treat the litter as the experimental unit.

Animals↗
PubMed1975

Induction and suppression of hepatic and extrahepatic microsomal foreign-compound-metabolizing enzyme systems by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on a number of hepatic and extrahepatic foreign-compound-metabolizing enzyme systems in microsomes from rats, rabbits and guinea pigs were investigated. Following TCDD treatment, the N-demethylation of benzphetamine, aminopyrine and ethylmorphine was suppressed in hepatic microsomes from male but not from female rats. However, both cytochrome P-450 and benzpyrene hydroxylase were significantly stimulated in hepatic microsomes from both male and female rats at doses as small as 1 mug TCDD/kg body weight. The inductive effect on rat hepatic microsomal enzymes was considerably more persistent than the suppressive effect. Following a single oral dose of 25 mug TCDD/kg weight, benzpyrene hydroxylase of male rat liver microsomes remained significantly elevated for 73 days but the suppression of benzphetamine N-demethylase had gone after 35 days. The induction of benzpyrene hydroxylase in male rat liver microsomes by TCDD was independent of the age of the rat and the levels to which this enzyme was increased was similar in male rats of all ages. However, the suppression of benzphetamine N-demethylase in male rat liver microsomes was age related: the suppression was seen only in adult animals and in the very young (10 days old) the enzyme was actually induced by TCDD. Inductive effects appeared in both smooth and rough-surfaced hepatic microsomes from male rats but the suppression of N-demethylation occurred only in the smooth-surfaced microsomes (SER). In microsomes from extrahepatic tissues of the rat, induction of mixed-function oxidases (MFOs) by TCDD occurred only in the kidney. However, UDPglucuronyltransferase was induced in microsomes from lung, kidney, intestine and brain but not testes. The response in the rabbit and guinea pig to TCDD differed considerably from that in the rat. Benzpyrene hydroxylase was unaffected in hepatic microsomes from the guinea pig and actually suppressed in microsomes from rabbit liver. Benzphetamine N-demethylase was also suppressed in rabbit liver microsomes. Glucuronyl-transferase was unaffected by TCDD in microsomes from liver, lung or kidney of the rabbit and guinea pig. The only lung enzyme responsive to TCDD was biphenyl 4-hydroxylase of the rabbit and guinea pig. Suppression was not observed in any of the extraheptic tissues studied and may be confined to only certain hepatic systems.

Animals↗
PubMed1975

Inhalation studies of nickel sulfide in pulmonary carcinogenesis of rats.

Two hundred twenty-six specific pathogenfree male and female F344 rats were exposed to nickel sulfide inhalations for 78 weeks (5 days/wk, 6 hr/day) and observed for an adiditional 30-week period. For the same amount of time, 214 rats were exposed to filtered room air and served as controls. Rats exposed to nickel sulfide showed a significantly higher incidence of pulmonary hyperplastic and neoplastic lesions originating from the bronchial and bronchiloo-alveloar segments. The overall incidence of lung tumors in the animals treated with nickel sulfide was 14 percent compared with 1 percent in the controls. Pulmonary inflammatory reactions were also greatly increased. Injection of an agent (hexachlorotetra-fluorobutane) that induced lung infarction did not increase the proportion of animals having lesions, nor did it alter the type of lesions found in animals exposed to nickel sulfide.

Animals↗
PubMedDate not supplied

Carcinogenicity of glycidol in F344 rats and B6C3F1 mice.

Glycidol, a simple aliphatic epoxide, was administered by gavage in water to groups of male and female F344/N rats and B6C3F1 mice. Rats received 0, 37.5 or 75 mg kg-1 and mice received 0, 25 or 50 mg kg-1 daily, 5 days per week for 2 years. Exposure to glycidol was associated with dose-related increases in the incidences of neoplasms in numerous tissues in both rats and mice. Survival of rats that received glycidol was markedly reduced compared to the control because of the early induction of neoplastic disease. In male rats, mesothelioma arising in the tunica vaginalis and frequently metastasizing to the peritoneum were considered the major cause of early death. Early deaths in female rats were associated with mammary gland neoplasms. Survival of female mice that received 50 mg kg-1 was lower than the control after week 101 due primarily to euthanasia of moribund animals with mammary gland neoplasms. Survival of male mice and female mice that received 25 mg kg-1 was comparable to the control. In mice, exposure to glycidol was associated with increased incidences of neoplasms of the harderian gland in males and females, the forestomach in males and the mammary gland in females.

1-Propanol↗