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Biomedical subjects

D B Menzel

Publications and source records attributed to D B Menzel.

At least 55 records · Page 3Linked to original sources
PubMed1980

Ozone induced alterations in phenol red absorption from the rat lung.

The effect of inhaled ozone (O3) on the integrity of lung transport processes for phenol red has been determined. Phenol red (1, 10, or 100 mumol) was applied intratracheally to rat lungs in vivo and in an isolated lung preparation. In both test systems the rates of removal were found to be similar and to compare favorably with reported values. Animals exposed to O3 for 24 h demonstrated loss of carrier-mediated transport for this ion. The effect was also found to be related to the concentration of O3. These results indicate that the carrier-mediated component of phenol red removal from the airways of the lung may be used as a marker for pulmonary membrane damage resulting from the inhalation of atmospheric toxicants.

Absorption↗
PubMed1979

Nasopharyngeal removal of ozone in rabbits and guinea pigs.

In estimating pollutant concentrations responsible for observed pulmonary effects, nasopharyngeal removal of the pollutant plays an important role. The nasopharyngeal removal of ozone (O3) in anesthetized male guinea pigs and male and female rabbits was determined by drawing O3 through the isolated upper airways at a constant flow rate which approximated the animal's respiratory minute volume. The tracheal O3 concentration in rabbits and guinea pigs was markedly similar and was linearly related to the chamber concentration of O3 over a range of 196--3920 micrograms/m3 (0.1--2.0 ppm O3). Regression analyses showed that O3 removal in the nasopharyngeal region is approximately 50% in both species. Both rabbit sexes responded similarly over the concentration range studied. Exposures of guinea pigs to O3 concentrations between 3920 and 5880 micrograms/m3 (2.0 and 3.0 ppm) showed that, at these higher concentrations, relatively more O3 is removed by the upper airways.

Animals↗
PubMed1979

Effect of dietary fat and vitamin E on mouse lung lipids.

To examine the effect of dietary fat on lung lipids, male weanling mice (CD-1 strain) were fed purified diets containing 5% stripped lard or corn oil and kept in chambers supplied with air filtered free of airborne bacteria. Vitamin E was fed at 0, 10.5 or 105 mg dl-alpha-tocopheryl acetate/kg diet. Dietary fat and vitamin E (0 or 10.5 mg/kg) had no significant effects on the lung levels of triacylglycerol (TG) or phospholipid (PL) molecular species through 4 weeks of intake. Alterations in lung fatty acid composition were followed through 6 weeks of intake at 0, 10.5 and 105 mg vitamin E/kg diet. Vitamin E, at all levels of supplementation, had no significant effect on mouse lung fatty acid composition. Saturated fatty acids of the lung also showed little alteration by diet, but feeding the lard diet significantly elevated oleic and palmitoleic acids. In mice fed the corn oil diet the levels of linoleic acid (18:2) were twice those of lard-fed mice, and arachidonic acid (20:4) was elevated by 15.8%. The diet elevated the mean peroxidizability index (PI) on lung tissue in corn oil-fed mice.

Animals↗
PubMed1979

Nutritional needs in environmental intoxication: vitamin E and air pollution, an example.

Dietary vitamin E affects the susceptibility of mice and rats to ozone and nitrogen dioxide, suggesting a free radical mechanism of toxicity. Conventional peroxidation does not completely explain the effects of alterations of lung fatty acid composition on both nitrogen dioxide and ozone toxicity. A new scheme is proposed based on the cyclization of beta, gamma-allylic peroxyl free radicals to monocyclic and bicyclic peroxides to explain the relationship between diet and toxicity. Similar results are likely with other toxicants producing peroxidation as a mechanism of toxicity. Such cyclic peroxides may mimic or interfere with the prostaglandin system. Several chronic diseases may be exacerbated through such a subtle toxic mechanism. The level of vitamin E needed for protection against peroxidation toxicity may be much greater than the present U. S. dietary intake.

Air Pollutants↗
PubMed1978

Mechanisms of lipid peroxidation: iron catalyzed decomposition of fatty acid hydroperoxides as the basis of hydrocarbon evolution in vivo.

Ethane and pentane are evolved during peroxidation of tissue lipids in vivo and are believed to be derived from omega3 and omega6 fatty acids respectively. We present evidence supporting a scission mechanism as the means of forming these hydrocarbons during hydroperoxide decomposition. A fatty acid omega6 hydroperoxide (methyl 13-hydroperoxy-6,9,11-octatrienoate), when incubated with a ferrous ion, yielded pentane as the major hydrocarbon (98%). Reaction with ferrous ion results in an alkoxy capable of undergoing scission to an aldehydic fatty acid and a hydrocarbon.

Catalysis↗
PubMed1978

Chemiluminescence of phagocytic cells caused by N-formylmethionyl peptides.

N-formylmethionyl (F-Met) peptides, when added alone to macrophages or polymorphonuclear leukocytes (PMN), were found to induce a chemiluminescent response of shorter duration than that produced by the commonly employed particulate stimulant, zymosan. The cellular nature of F-Met peptide-induced chemiluminescence was indicated by its dependence on cell concentration, and by its inhibition by cell disruption, heat inactivation, or previous maximal stimulation by the peptides. Comparison of PMN and macrophages from different species showed that the maximal chemiluminescent response seen in the dose-response curve of F-Met- Phe was different in different cell types. Chemiluminescence reached highest values in human PMN, it was intermediate in guinea pig macrophages and PMN, and in rabbit PMN; but it was nonexistent in rabbit alveolar macrophages and very low in rabbit peritoneal macrophages. A definite relationship was observed between peptide structure and chemiluminescent activity. Met-Phe, F- Met and Phe were inactive even at millimolar concentrations, while F-Met-Phe caused chemiluminescence at micromolar concentrations. Four active peptides were tested in guinea pig, rabbit, and human PMN, and in guinea pig alveolar and peritoneal macrophages. The relative activity of these peptides was the same in all cells studied, e.g. F-Met-Leu-Phe >> F-Met-Phe > F-Met-Val > F- Met-Ala. The values of ED50 for each peptide were also comparable to previously reported ED50 values of these peptides in inducing lysosomal enzyme release. These results were seen both in the presence and absence ofthe chemiluminescent oxidant indicator, luminol. Low concentrations of superoxide dismutase (10 mug/ml) completely inhibited chemiluminescence caused by the F-Met peptides, suggesting the involvement of 0(2)(-) or O(2)(-)-derived compounds in this response. Sodium azide, an inhibitor of peroxidase reactions, had either no effect or a slight inhibitory effect on chemiluminescence. However, when the extracellular release of lysosomal enzymes was induced by cytochalasin B, an azide- inhibitable enhancement of chemiluminescence was seen in PMN, but not in macrophages. This effect appears to be correlated with the presence of granule-associated myeloperoxidase. Although azide-inhibitable peroxidases could be a potential source of light, they did not appear to be a significant contributor in these experiments. Based on these results and on those of previous investigators, we postulate that the F-Met-peptides stimulate 0(2)(-) production in addition to stimulating lysosomal enzyme release and chemotaxis. The similar structure- activity relationship which appears to exist for these processes may indicate that they are all initiated by a single receptor mechanism. Since F-Met peptides are formed in bacteria it is likely that their actions represent an important physiologic response.

Animals↗
PubMed1978

Similarity between man and laboratory animals in regional pulmonary deposition of ozone.

Predicted pulmonary ozone (O3) dose curves obtained by model analysis of the transport and removal of O3 in the lungs of guinea pigs, rabbits, and man indicate that a general similarity exists among these species in the shapes of the dose curves. An overview of the major features of the lower airway mathematical model used is presented. This model predicts that the respiratory bronchioles receive the maximum O3 dose. For exposures corresponding to tracheal O3 concentrations greater than 100 micrograms/m3 (0.05 ppm), the predicted respiratory bronchiolar dose for rabbits was found to be twice that for guinea pigs and 80% of that for man. Sensitivity analyses are presented for model parameters relating to the treatment of the chemical reactions of O3 with the mucous layer. The role of tidal volume in the determination of pulmonary uptake of O3 in man is examined. The consistency and similarity of the dose curves for the three species lend strong support to the validity of extrapolating to man the results obtained on animals exposed to O3.

Animals↗
PubMed1978

Absorption of paraquat and diquat from the airways of the perfused rat lung.

The uptake of paraquat dichloride (bis-N-[14C]methyl-4,4'-bipyridilium chloride) and diquat dibromide (N,N-ethylene-[U-14C]2,2'-bipyridilium dibromide monohydrate) from the airways and by the vasculature of the isolated and perfused rat lung (IPL) were studied. A semilogarithmic plot of the percent unabsorbed with time revealed a bi-exponential decay, suggesting at least two phases of removal of paraquat and diquat from the airways. The rapid initial process was similar for both herbicides. The slow component had at t1/2 of 355.98 min for paraquat and 75.03 min for diquat. This second process may represent the storage pool associated with the pulmonary toxicity of paraquat. When paraquat or diquat was presented to the capillary side of the lung, long-term storage was not evident. Uptake by the lung occurred from the pulmonary circulation with similar velocity. These data suggest that the energy-dependent uptake observed with lung slices probably represents airway transport and may be associated with cell membranes lining the alveolus.

Absorption↗
PubMed1976

DDT: the degradation of ring-labeled 14C-DDT to 14CO2 in the rat.

Ring fission of p, p'-DDT was studied in the rat following a single oral dose of 0.74 mg/kg (1.04 muCi) of uniformly ring-labeled 14C-DDT. Expired air was passed through a solution of ethanolamine-ethylene glycol monomethyl ether (1:2) to trap 14CO2. A total of 1.6% of the radioactivity administered was recovered in the expired air collected continually for 10 days, indicating that while degradation of the phenyl moiety is not a major route of p,p'-DDT metabolism in the rat, it is equal to the urinary excretion. Nevertheless, these results represent the most radical change accomplished in vivo of a residual insecticide yet reported in mammals.

Animals↗