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Biomedical subjects

C E Cross

Publications and source records attributed to C E Cross.

At least 145 records · Page 8Linked to original sources
PubMed1977

Lactate dehydrogenase activity and isoenzyme pattern in lungs, erythrocytes, and plasma of ozone-exposed rats and monkeys.

The effect of low levels of ozone exposure (8 hr daily for 7 days) on lactate dehydrogenase (LDH) activity and isoenzyme pattern was studied in the lungs, plasma, and erythrocytes of rats and monkeys. Exposure to 0.8 or 0.5 ppm ozone resulted in a significant increase in total LDH activvity in the lungs but not in the plasma and erythrocytes of rats. The LDH-5 fraction of the LDH isoenzymes was significantly decreased in terms of percentage distribution in the lungs and plasma of rats exposed to 0.8 ppm ozone, whereas the LDH-4 in the lungs and plasma and LDH-3 in the lungs were increased. At 0.5 ppm ozone, the isoenzyme distribution was not significantly changed in lungs, plasma, or erythrocytes. In monkeys, no significant change in either total LDH activity or isoenzyme pattern was observed in lungs, plasma, or erythrocytes after exposure to 0.8 ppm ozone.

Animals↗
PubMed1977

Glycoprotein secretion by tracheal explants cultured from rats exposed to ozone.

Tracheal explants from rats exposed to 0.8 ppm (1.9 mg per m3) of ozone 8 hours per day for 1 to 90 days were incubated in culture with glucosamine labeled with carbon-14 or hydrogen-3. Compared with tracheas from control rats exposed to filtered air, the explants demonstrated a decreased rate of glycoprotein secretion for exposure intervals of as long as one week, followed by a rebound to an increased rate of glycoprotein secretion for at least 12 weeks of continued exposure to ozone. Detailed study of the behavior of labeled glycoproteins from the culture medium on chromatography on columns of BioGel A-150m demonstrated that the ratio of the low to high molecular weight peaks increased when there was an increased rate of glycoprotein secretion. This is the first report of a direct biochemical effect induced by ozone on airway metabolism.

Air Pollutants↗
PubMed1977

Enhanced lung toxicity of O2 in selenium-deficient rats.

To test the hypothesis that glutathione (GSH) peroxidase is an important component of the lung's anti-oxidant defense systemes, O2 toxicity was studied in selenium (Se)-deficient rats. Chronic respiratory disease free rats fed a Se-deficient diet or a diet supplemented with Se for 40 days after weaning were exposed to 80% O2 at atmospheric pressures for 3 days. Activities of GSH peroxidase in lungs of Se-deficient rats were markedly lower than corresponding activities in rats supplemented with 0.5 or 2.0 ppm Se. With O2 exposure, 35% of the rats fed the Se-deficient regimen died, whereas all rats fed Se-supplemented diets survived. Lungs from surviving Se-deficient rats exposed to O2 were edematous. The data suggest that the toxic effects of O2 are enhanced in Se-deficient rats and that nutritional factors contribute to lung susceptibility to oxidant-induced damage.

Animals↗
PubMed1976

Oxygen toxicity: augmentation of antioxidant defense mechanisms in rat lung.

In studies directed at determining the activities of selected enzymes in lung tissue after in vivo exposure to hyperoxia, 70-day-old rats were exposed to 85% or 90% O2 for 1-14 days. After 7 days of exposure to 90% O2 (1atm), superoxide dismutase activities in mitochondrial and cytosolic fractions increased, respectively, to 245 and 145% of control; glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities increased, respectively, to 317, 175, and 413% of control. The levels of reduced glutathione and total nonprotein sulfhydryl compounds were elevated to 195% and 365% of control. Similar changes were observed in rats exposed to 85% O2 for up to 14 days, but to a lesser degree. The changes are interpreted as a reflection of the overall magnitude of oxidant-induced lung injury-reparative processes. The results suggest that hyperoxia induces an increase in lung "antioxidant" defense capabilities. This apparent adaptive response may be important in decreasing the susceptibility of lung tissue to continued O2 toxicity.

Animals↗
PubMed1975

Ozone interaction with rodent lung. III. Oxidation of reduced glutathione and formation of mixed disulfides between protein and nonprotein sulfhydryls.

Nonprotein sulfhydryls (NPSH), a major source of cellular reducing substances, were examined in lung tissue after short-term exposure of rats to O3. While the NPSH level was unaffected by low-level exposures (e.g., 0.8 ppm for up to 24 h or 1.5 ppm for up to 8 h), it was significantly lowered by higher exposure regimens (e.g., 25 per cent after 2 ppm for 8 h and 49 per cent after 4 ppm for 6 h). After exposure to 4 ppm O3 for 6 h the level of reduced glutathione (GSH), which accounted for approximately 90 per cent of NPSH in the lung, decreased 40 per cent but without a rise in the level of oxidized gluathione (GSSG). Treatment of lung homogenate with borohydride led to recovery of NPSH in exposed lungs to control values, suggesting that NPSH or GSH oxidation during in vivo O3 exposure resulted in formation of mixed disulfides with other sulfhydryl (SH) groups of lung tissue. Extracts of borohydride-treated particulate and supernatant fractions of lung homogenate were analyzed for NPSH by paper chromatography. From this analysis GSH appeared to be the only NPSH bound to lung tissue proteins via mixed disulfide linkage. The formation of mixed disulfides appeared to be a transient phenomenon. Immediately after a 4-h exposure to 3 ppm O3 the level of mixed disulfides was small (15 per cent of the total NPSH) but attained a peak (equivalent to 0.6 mumol NPSH/lung) after a recovery for 24 h. However, the level diminished considerably within 48 h of recovery.

Animals↗
PubMed1975

Effects of ozone exposure on the lungs and the erythrocytes of rats and monkeys: relative biochemical changes.

Ozone exposure (0.5 p.p.m., 8 hours daily for 7 days) resulted in a 20-26% (P less than 0.05) increase in the level of reduced glutathione (GSH), and the activities of the GSH peroxidase system in rat lungs. The increases were of smaller magnitude (10-15%) in the lungs of ozone-exposed monkeys. No significant changes were observed in these parameters in the erythrocytes of ozone-exposed and control animals of the two species. The results suggest that rats may be more sensitive to ozone than monkeys in terms of biochemical lesions in the lung, and that ozone effects are manifested primarily in the lung.

Animals↗