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Biomedical subjects

T R Tyler

Publications and source records attributed to T R Tyler.

49 records · Page 3Linked to original sources
PubMed1984

Acute and subchronic toxicity of ethylene glycol monobutyl ether.

The available information on the acute and subchronic toxicity of ethylene glycol monobutyl ether is reviewed. Data from animal studies have been examined from the standpoint of dose-response relationships and the sensitivity of various animal species, including man, to the effects of this chemical. In view of recent findings with other chemically related glycol ethers, particular attention has been given to possible adverse effects on blood and testicular tissue. In evaluating the hazard that this chemical may pose to man, consideration has been given to likely routes of exposure and its irritant properties. It is concluded that the available information continues to support the current ACGIH TWA8-TLV of 25 ppm with a STEL of 75 ppm.

Administration, Topical↗
PubMed1983

Media and agenda setting: effects on the public, interest group leaders, policy makers, and policy.

Using an experimental design built around a single media event, the authors explored the impact of the media upon the general public, policy makers, interest group leaders, and public policy. The results suggested that the media influenced views about issue importance among the general public and government policy makers. The study suggests, however, that it was not this change in public opinion which led to subsequent policy changes. Instead, policy change resulted from collaboration between journalists and government staff members.

Chicago↗
PubMed1978

Ionic milieu of bovine and ovine rumen as affected by diet.

Postprandial changes in osmolality, mineral, and volatile fatty acid concentrations in rumen fluid were examined in three cattle fed six widely differing diets. Mineral concentrations varied with diet and postprandial time. However, net changes in postprandial mineral concentrations did not contribute significantly to changes in osmotic pressure. There was an effect of diet and time after feeding on concentrations of volatile fatty acids. Postprandial changes in osmotic pressure were primarily due to changes in concentrations of volatile fatty acids. Magnesium oxide and sodium bicarbonate were fed to sheep to increase the osmotic pressure in rumen fluid. The salt supplement decreased acetate, propionate, heat, and methane production. However, rumen water flux was unaffected by the salt supplementation. Diets which produce hypertonic rumen fluid due to high mineral and/or concentrations of volatile fatty acids may reduce fermentation in rumen.

Animal Feed↗
PubMedDate not supplied

Pharmacokinetics and material balance studies of diethylenetriamine trihydrochloride in the Fischer 344 rat following oral, endotracheal or intravenous dosing.

The metabolism and disposition of diethylenetriamine trihydrochloride (DETA.3HCl) were studied with regard to route of administration and dosage effects. Male Fischer 344 rats were administered 50 or 500 mg kg(-1) of [1,2-(14)C]-DETA.3HCl orally or endotracheally, and the fate of the 14C-radioactivity was followed for 48 h. The DETA.3HCl was readily absorbed from the gut or the lung, with bioavailabilities of 95% and 90%, respectively. It was distributed throughout the body, with the kidney attaining the highest concentration (about 2.5-5 times that of blood). The apparent volume of distribution determined from plasma concentration data following intravenous dosing (50 mg kg[-1]) was 486 ml kg(-1), consistent with distribution in the total body water. Urine and feces were the major routes of excretion, with only a small fraction eliminated as CO2. Excretion was quite rapid, with over 96% of the dose eliminated within 48 h. The principal component in the urine was unchanged DETA, suggesting that DETA.3HCl was not extensively metabolized. While the major metabolites has not been identified, there was evidence that DETA.3HCl was neither metabolized to ethylenediamine nor to the acid conjugates. There was indication that the metabolism of DETA.3HCl was saturated at 500 mg kg(-1), as there was a shift to a higher proportion of unchanged DETA excreted in the urine. There were no significant differences in material balance or pharmacokinetic parameters among animals receiving DETA.3HCl by the oral or endotracheal routes of administration.

Administration, Oral↗
PubMedDate not supplied

Subchronic inhalation neurotoxicity study of amyl acetate in rats.

An inhalation toxicity study was conducted with rats to examine the potential for amyl acetate vapor to produce alterations in nervous system structure and function following repeated exposure. The study was performed as part of a USEPA Toxic Substances Control Act (TSCA) Section 4e Enforceable Consent Agreement for amyl acetate. Rats (CD) were exposed to amyl acetate vapor at concentrations of 0, 300, 600 or 1200 ppm, 6 h per day, 4 or 5 days per week, for at least 65 exposures. Treatment groups consisted of 15 rats per gender for the control and 1200 ppm groups and 10 rats per gender for the 300 and 600 ppm groups. Evaluations included clinical observations before, during and after each exposure, weekly detailed clinical examinations, weekly body weight and food consumption measurements and monthly functional observational battery and motor activity measurements conducted on non-exposure days. Neuropathology examination of the central and peripheral nervous system was performed at the end of the study. Exposure to amyl acetate did not result in overt clinical signs of toxicity or changes in body weight or food consumption. Transient, subtle decreases in general activity level during the 6-h exposure period were noted for animals in the 600 and 1200 ppm groups during the first 2 weeks of the study. Functional observational battery evaluations, automated motor activity measurements and neuroanatomy were unaffected by exposure. The no observed-effect level for subchronic neurotoxicity for this study was at least 1200 ppm, which is greater than an order of magnitude above the occupational threshold limit value (8-h, time-weighted average) for amyl acetate (100 ppm).

Administration, Inhalation↗
PubMedDate not supplied

Isopropanol: acute vapor inhalation neurotoxicity study in rats.

Five groups of 25 Fischer 344 rats of each sex were exposed for 6 h to isopropanol vapor at 0, 500, 1500, 5000 or 10,000 ppm. Behavioral observations for 10 rats of each sex were made prior to and 1, 6, and 24 h after exposure. Motor activity was evaluated for 15 rats of each sex prior to and immediately following exposure. Exposure to isopropanol caused a spectrum of transient effects indicative of narcosis at 10,000 ppm and sedation at 5000 ppm. Prostration or severe ataxia, decreased arousal, slowed or labored respiration, decreased neuromuscular function, hypothermia and loss of reflex function were observed 1 and 6 h after exposure to 10,000 ppm isopropanol vapor. Similar, but less severe, alterations were observed in animals in the 5000 ppm exposure group 1 h after exposure. Exposure concentration-related decreases in motor activity were observed in males and females in the 5000 and 10,000 ppm groups and slight decreases in motor activity were observed in males in the 1500 ppm group. Animals in the 1500 and 5000 ppm exposure groups recovered from these motor activity effects within 5 h. Based on this study, exposure of male and female rats to isopropanol vapor produces transient, concentration-related narcosis and/or sedation at concentrations of 5000 and 10,000 ppm and minor decreases in motor activity in males at a concentration of 1500 ppm. The no-observed-effect level (NOEL) for this was 500 ppm isopropanol.

1-Propanol↗
PubMedDate not supplied

Two-generation reproduction toxicity study with isopropanol in rats.

A two-generation reproduction toxicity study was conducted in rats with isopropanol. Thirty rats of each sex per group (P1) were dosed once daily by oral gavage with 0, 100, 500 or 1000 mg isopropanol kg-1 for at least 10 weeks prior to mating. Parental animals were mated within groups for up to 3 weeks. Parental females were dosed during mating, gestation and lactation; parental males were dosed during mating through delivery of their last litter sired. The P2 adults were selected from the F1 litters and were dosed for 10-13 weeks before mating to produce a single litter. Findings in the parental animals included increased lactation body weight gain in the mid- and high-dose females, increased liver and kidney weights in the mid- and high-dose groups of both sexes and centrilobular hepatocyte hypertrophy in some P2 males. There was also accumulation of hyaline droplets and other microscopic findings in the kidneys from the mid- and high-dose P1 males and from all treated groups of the P2 males. Increased mortality was observed in the high-dose F1 offspring during the early postnatal period, although no other clinical signs of toxicity were observed in the offspring of either generation. In addition, offspring body weight was reduced during the early postnatal period in the high-dose F1 males and in the high-dose F2 pups of both sexes. Eighteen out of 70 F1 weanlings in the 1000 mg kg-1 group died or were euthanized prior to P2 selection. No treatment-related post-mortem findings were observed in the offspring from either generation.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Propanol↗
PubMedDate not supplied

Identification of a glutathione conjugate of cambendazole formed in the presence of liver microsomes.

The incubation of multiply labeled (2H, 3H, 13C, 14C) cambendazole and glutathione with hepatic microsomes from phenobarbital-dosed hamsters results in the formation of polar metabolites. The major metabolite has been characterized by a variety of isotopic, spectrometric, chromatographic, and degradative/synthetic techniques as a glutathione conjugate of cambendazole in which substitution is on the 4-position of the benzimidazole nucleus. The same metabolite is produced by hepatic microsomes from the rat.

Animals↗