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Biomedical subjects

S G Jenkinson

Publications and source records attributed to S G Jenkinson.

At least 73 records · Page 4Linked to original sources
PubMed1984

Glutathione peroxidase, superoxide dismutase, and glutathione S-transferase activities in human lung.

Glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and glutathione S-transferase activities were measured in lung tissue obtained from 7 patients receiving resectional surgery because of localized lung tumors. Human-lung-soluble fractions were also fractionated on Sephadex G-150-S columns, and GSH-Px activity was measured using hydrogen peroxide and cumene hydroperoxide as substrates to investigate the presence of non-selenium-dependent GSH-Px activity. The amount of SOD activity was found to be similar to the amount of activity present in rat lung. Glutathione S-transferase activity was 3 times greater in human lung than that in rat lung. Selenium-dependent GSH-Px activity was much lower in human lung than that in rat lung (less than 30%), and no evidence of non-selenium-dependent glutathione peroxidase activity was found in human lung using gel filtration techniques. We conclude that human lung differs from rat lung in some antioxidant enzymatic defense mechanisms, and that selenium deficiency could result in marked decreases in the ability of human lung to detoxify organic hydroperoxides.

Animals↗
PubMed1984

Endotoxin protects selenium-deficient rats from hyperoxia.

Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.

Animals↗
PubMed1983

Non-selenium-dependent glutathione peroxidase activity in rat lung: association with lung glutathione S-transferase activity and the effects of hyperoxia.

To determine if non-selenium-dependent glutathione peroxidase (Non-Se GSH-Px) activity is present in rat lung, we fractionated rat lung soluble fractions from rats fed a selenium-deficient or control diet and measured glutathione peroxidase activity with both cumene hydroperoxide and hydrogen peroxide as substrates. We also measured glutathione S-transferase (GSH S-transferase) activity in the fractions with 1-chloro-2,4-dinitrobenzene as substrate. Non-Se GSH-Px activity was present (about 34% of total GSH-Px activity), and the peak present in the gel filtration chromatogram coeluted with the GSH S-transferase peak. We then measured GSH S-transferase activity in lung-soluble fractions from rats exposed to room air or 85% O2 for 5 days. Lung GSH S-transferase activity was increased in the oxygen-exposed animals when compared to the air-exposed controls. The increase in GSH S-transferase activity could represent the induction of lung non-Se GSH-Px activity.

Animals↗
PubMed1982

Effects of copper deficiency on the activity of the selenoenzyme glutathione peroxidase and on excretion and tissue retention of 75SeO3(2-).

Liver and lung activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were determined in control and copper-deficient rats. Decreased activity of SOD was found in liver and decreased activity of the selenoenzyme GSH-Px was found in liver and lung in the copper-deficient animals. The decreased liver activity of GSH-Px could be partially corrected by daily supplementation of the basal diet with sodium selenite. Urinary, fecal and biliary excretion of 75SeO3(2-) were determined in controls and copper-deficient rats in order to assess selenium losses. Urinary excretion of 75Se was not different in the two groups. Fecal loss of 75Se was increased in the copper-deficient animals when compared to controls and biliary excretion was decreased. Tissue retention of 75Se was also determined in both groups. Retention of 75Se in the copper-deficient rats was increased in brain and lung and decreased in liver. This pattern of tissue retention of 75Se is similar to that which occurs in selenium-deficient rats. Copper deficiency in rats results in decreased liver activity of both the copper-containing enzyme SOD and the selenoenzyme GSH-Px. The mechanism of decreased GSH-Px activity is unknown.

Animals↗
PubMed1982

Radioimmunoassay determinations of prostaglandin E in pleural effusions of varying causes.

The concentrations of prostaglandin E (PgE) were measured in pleural fluid samples from 26 consecutive patients with pleural effusions of varying causes. The PgE concentrations were significantly increased in exudates when compared with transudates and provided a single measurement to separate these 2 classifications of pleural fluid. The highest concentrations of PgE were found in exudates associated with tuberculous pleuritis and metastatic lung cancer. Simultaneous measurement of pleural fluid and plasma PgE concentrations in patients with malignant effusions revealed that pleural fluid concentrations did not reflect plasma concentrations.

Adult↗
PubMed1982

Inability of niacin to protect from in vivo hyperoxia or in vitro microsomal lipid peroxidation.

The efficacy of niacin in protecting rats from normobaric hyperoxia was evaluated in vivo by exposing niacin treated animals and controls to greater than 95% O2 for 96 hours. The vitamin was also evaluated as a possible free radical scavenger in vitro using an Fe-ascorbate initiated microsomal lipid peroxidation system. No protective effects were observed in vivo either in mortality or in differences in lung wet and dry weights of the niacin treated rats when compared to controls. Niacin in varying concentrations also did not decrease lipid peroxidation in the microsomal systems. Although this vitamin has been reported to protect animals from paraquat toxicity when given intraperitoneally once daily, niacin administered in similar doses does not appear to protect rats from hyperoxia.

Animals↗
PubMed1981

Hepatic cytochrome P-450 and microsomal heme oxygenase in copper-deficient rats.

Copper deficient and control rats were pair-fed from weaning a milk-based diet. Each animal received 25 mg of iron parenterally. After 6 weeks of dietary manipulations the animals were killed. As expected, rats fed the copper-deficient diet were anemic. Copper-dependent enzyme activities and copper content of plasma and liver confirmed that copper deficiency was present in these rats. Hepatic microsomal cytochrome P-450 specific contents were similar in control and copper-deficient animals in the uninduced state and following induction of cytochrome P-450 by treatment with phenobarbital. However, microsomal heme oxygenase was increased in copper-deficient animals compared with controls whether they were treated with phenobarbital or not. No differences were observed in splenic microsomal heme oxygenase between dietary groups. These studies suggest that hepatic heme catabolism is enhanced in copper deficiency. The explanation for this enhancement may be related to increased hepatic iron accumulation in copper-deficient animals or to the associated defect of selenium metabolism in copper deficiency.

Animals↗
PubMed1980

Parapneumonic effusions.

In this study the incidence and course of pleural effusions (parapneumonic effusions) in patients with acute bacterial pneumonia were prospectively evaluated. Bilateral decubitus chest x-ray films were obtained within 72 hours of admission in 203 patients with an acute febrile illness, purulent sputum and an infiltrate evident on the chest film. Ninety of the 203 patients (44 percent) had pleural effusions. Parapneumonic effusions, which required chest tubes for resolution and/or on which the pleural fluid cultures were positive, were classified as complicated parapneumonic effusions. The 10 patients with complicated parapneumonic effusions had clinical characteristics similar to the remainder of the group and could be separated from the 80 with uncomplicated effusions only by pleural fluid analysis. A pleural fluid pH below 7.00 and/or a glucose level below 40 mg/100 ml are indications for immediate tube thoracostomy. In patients with pleural fluid pH between 7.00 and 7.20 or lactic dehydrogenase (LDH) above 1,000 IU/1,000 ml, tube thoracostomy should be considered, but each case should be individualized; serial studies of the pleural fluid are useful in some of these cases. Patients with pleural fluid pH above 7.20 and pleural fluid LDH below 1,000 mg/100 ml rarely have complicated parapneumonic effusions and do not require serial therapeutic thoracenteses.

Adult↗
PubMed1980

Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis.

In 52 patients with pleural effusions, pleural pressures were measured initially and serially as pleural fluid was withdrawn. Pleural fluid aspiration was continued until the pleural pressure fell below -20 cmH2O, or the patient developed excessive symptoms, or no more fluid could be obtained. The initial pleural pressure ranged from +8 to -21 cmH2O. The rate of pleural pressure change as fluid was withdrawn was highly variable. In 13 of 52 procedures (25%), thoracentesis was terminated because the pressure fell below -20 cmH2O. Negative initial pleural pressures and/or rapid changes in the pressures as fluid was withdrawn were suggestive of malignancy or trapped lung. The measurement of pleural pressures in patients with pleural effusions may be useful diagnostically. More importantly, because large changes in pleural pressures are not readily detectable by the operator, pleural pressures should be monitored when large amounts (> 1,000 ml) of pleural fluid are removed to increase the safety of the procedure.

Drainage↗
PubMed1980

Serial pulmonary function studies in survivors of near drowning.

Determinations of standard lung volumes, mechanics of breathing, and single breath carbon monoxide diffusing capacity (DLCO) were obtained serially in two young patients who survived near drowning in fresh water. These patients were nonsmokers and neither had a past history of lung disease. Pulmonary function studies in both patients revealed a restrictive ventilatory defect with a decreased forced vital capacity and total lung capacity. One patient also exhibited a markedly decreased DLCO. No obstructive lung disease was found in either case. All pulmonary function abnormalities returned to normal during the 16 week follow-up period. Near drowning in fresh water did not cause permanent pulmonary dysfunction in these two young patients.

Adolescent↗
PubMed1979

Cefazolin vs penicillin. Treatment of uncomplicated pneumococcal pneumonia.

Cefazolin sodium, 500 mg intramuscularly twice daily, was compared with penicillin G procaine, 600,000 units intramuscularly twice daily, in the treatment of 82 patients with pneumococcal pneumonia. Patients were randomly assigned except when there was a history of penicillin allergy. The patients received treatment for five days or until they were afebrile for 48 hours. No patients experienced side effects or allergic reactions. All patients recovered satisfactorily without relapses. Cefazolin in the previously described dosage is as effective as penicillin in the treatment of pneumococcal pneumonia.

Cefazolin↗