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Biomedical subjects

R T Drew

Publications and source records attributed to R T Drew.

64 records · Page 4Linked to original sources
PubMedDate not supplied

Effects of sulfur dioxide and ozone on hypertension sensitive and resistant rats.

Two lines of Dahl rats, one resistant to salt-induced hypertension (DR) and one susceptible to salt-induced hypertension (DS) were subchronically exposed to SO2 (50 ppm, 6 hr/d, 5 d/wk for 31 weeks) or ozone (2.0 ppm, 6 hr/d, 5 d/wk for 20 weeks). Subgroups of rats were maintained on either high or low salt diets. In rats not expected to develop hypertension, exposure to SO2 caused a slight but consistent decrease in blood pressure. In DS rats on a high salt diet exposure to SO2 resulted in an increase in blood pressure over that of their air exposed counterparts. All exposure-related differences in blood pressure disappeared after the last exposure to SO2. Exposure to ozone was fatal to all DS rats, regardless of the amount of salt in the diet. The DR rats were more resistant to ozone, with most animals surviving the 20-week exposure. Ozone-exposed rats exhibited a decrease in both growth rate and blood pressure in all groups when compared to their air-exposed counterparts. It is not known if exposure-related blood pressure differences would persist after ending ozone exposures. After brief exposures, ozone caused increased lung weights in both groups, but there were no consistent changes in pulmonary nonprotein sulfhydryl groups. Hepatic nonprotein sulfhydryl levels were consistently, but not significantly, lower in ozone-exposed rats.

Animals↗
PubMedDate not supplied

Role of exposure databases in risk management.

Despite the development of numerous national exposure-related databases, exposure assessment remains a weak link in the chain of risk assessment and risk-management activities. Most databases include measures of environmental releases or concentrations of pollutants in specific media, but do not include actual measures of exposure. If accurate estimates of exposure experienced by populations or individuals are absent, it is impossible to judge the effectiveness of risk-management strategies. The Risk Management Work Group evaluation identified the following needs: refinement of measurements of total exposure experienced by individuals, improved characterization of the distribution of exposures in the population, longitudinal monitoring of exposure trends, and improved information about the public health implications of exposure. Recommendations are presented with the hope that the utility of existing databases will be improved and that future initiatives will be developed that meet the needs of risk management.

Databases, Factual↗
PubMedDate not supplied

Species differences in benzene hydroxylation to phenol by pulmonary and hepatic microsomes.

The metabolism of benzene to phenol by microsomal preparations from lung and liver has been compared in hamsters, rats, and rabbits. There were wide differences in the apparent Vmax of benzene hydroxylation among the various species and tissues and smaller differences in the apparent KM values for benzene hydroxylase. Benzene can inhibit its own metabolism in vitro when present in high concentrations. Phenol was the only metabolite of benzene identified, under the conditions of the assay, in incubation mixtures containing microsomes from lung or liver of any of the three animal species. When incubated with microsomes under the conditions used to measure benzene metabolism, phenol was further metabolized in liver but not in lung preparations. Phenol metabolism was almost completely inhibited when 11.2 mM benzene was included in the incubation mixture containing hepatic microsomes. The variation in rates of benzene hydroxylation by microsomal preparations from lungs or livers of the three animal species was similar to the variation in rates of benzypyrene hydroxylation in the same preparations.

Aniline Hydroxylase↗
PubMedDate not supplied

The biotransformation of p-xylene to a toxic aldehyde.

Rats given a single ip injection of p-xylene suffered 65% loss of pulmonary microsomal p-xylene hydroxylase activity. The activity was protected by pretreating the rats with phenobarbital, which increased hepatic p-xylene hydroxylase and cytosolic aldehyde dehydrogenase activities, but had no effect on alcohol dehydrogenase activity in hepatic cytosol. Pretreatment of rats with pyrazole caused a 60% inhibition of liver alcohol dehydrogenase but had no effect on liver aldehyde dehydrogenase activity. This treatment partially protected the pulmonary microsomal p-xylene hydroxylase from inactivation by p-xylene. Experiments in vitro showed that inactivation of cytochrome P-450 by p-xylene required the metabolic conversion of p-xylene to p-tolualdehyde. The reactive intermediate (p-tolualdehyde) required the presence of NADPH to carry out the inactivation. Inasmuch as lung tissues cannot form p-tolualdehyde (because of the low activity of p-methylbenzyl alcohol dehydrogenase), it is assumed that the inactivation of lung enzymes in vivo following exposure to p-xylene was due to the aldehyde intermediate which is formed in the liver and transported to the lung.

Aldehydes↗