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Biomedical subjects

C E Cross

Publications and source records attributed to C E Cross.

186 records · Page 11Linked to original sources
PubMedDate not supplied

Ascorbic acid turnover in the mouse following acute ozone exposure.

Swiss Webster mice were continuously exposed to an atmosphere containing 1.5 ppm ozone (O3) for 5 days. Control mice breathed filtered air. Immediately following the exposure period each mouse was then injected with [1-14C] ascorbic acid. The rate of disappearance of [1-14C] ascorbic acid and the levels of total ascorbic acid were determined in serum, lung, liver, and the remaining carcass over a 9-day period. O3 exposure caused transient decreases in the ascorbic acid levels in liver and serum, whereas lung ascorbic acid levels increased. The apparent biological half-life of ascorbate in carcasses (minus lung and liver) from O3-exposed mice, was significantly prolonged. Significant changes were also observed in the net flux of ascorbic acid in all tissues examined. The results indicated that the change in ascorbic acid levels in a given tissue appeared to reflect changes in the rate of ascorbic acid degradation, its mobilization or tissue compartmentalization, rather than increased synthesis in response to O3 exposure.

Animals↗
PubMedDate not supplied

Base modification and strand breakage in isolated calf thymus DNA and in DNA from human skin epidermal keratinocytes exposed to peroxynitrite or 3-morpholinosydnonimine.

Exposure of isolated calf thymus DNA and human skin epidermal keratinocytes to peroxynitrite or the peroxynitrite generator, 3-morpholinosydnonimine (SIN-1), led to extensive DNA base modification. Large increases in xanthine and hypoxanthine, possible deamination products of guanine and adenine, respectively, and in 8-nitroguanine were observed, but only small changes in some oxidized base products were seen. This pattern of damage suggests that hydroxyl radicals were not major contributors to base modification caused by peroxynitrite, as OH is known to cause multiple oxidative modifications to all four DNA bases. Instead, it seems that reactive nitrogen species play a much greater role in the mechanism of base damage, producing both nitration and deamination of purine bases when DNA or whole cells are exposed to peroxynitrite. If this pattern of damage is unique to peroxynitrite, it might act as a marker of cellular damage by this species in vivo.

Animals↗
PubMedDate not supplied

Stimulation by cigarette smoke of glutathione peroxidase system enzyme activities in rat lung.

This study was undertaken to evaluate the effect of in vivo cigarette smoke exposure on glutathione peroxidase--related enzyme systems of the rat lung. These enzymes, acting in concert, are thought to be responsible for disposing of toxic lipid peroxides in pulmonary tissue. Thirty-day-old rats were exposed to thirteen cigarettes per day for 21 days with a Walton reverse-smoking exposure apparatus. After 21 days of smoke exposure, the activities of glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase were increased 34%, 24%, and 38%, respectively, over control values. This level of cigarette smoke exposure did not cause detectable histological lesions. We present the hypothesis that short-term, low-level cigarette smoke exposure is capable of initiating metabolic alterations in lung cells at exposures at which histological changes are not detectable by light microscopy.

Animals↗
PubMedDate not supplied

Biochemical effect of ozone exposure in rats exposed to cigarette smoke.

Rats were exposed to three cigarettes per day for 35 days, under realistic conditions. Pulmonary glucose-6-phosphate dehydrogenase (G-6-PD) activity in the exposed animals increased 27% over control values (P less than .05). Subsequent exposure to acute, high-dose ozone (3 ppm for 4 hr) decreased the augmented G-6-PD activities to near normal levels, whereas ozone exposures in animals not exposed to cigarette smoke caused mild decreases in pulmonary G-6-PD activities. The importance of these findings with respect to the susceptibility of the smoker to oxidant exposures is unknown.

Animals↗
PubMedDate not supplied

Canine chronic bronchitis. A pathophysiologic evaluation of 18 cases.

Eighteen dogs with chronic bronchitis were studied using physiologic, radiologic, microbiologic, and pathologic techniques. Twelve of these dogs were evaluated before and after two weeks of oral bronchodilator administration. Thoracic radiographs, tidal breathing flow-volume loops, radioaerosol ventilation scans, airway appearance at bronchoscopy, and airway pathology were abnormal in the majority of dogs studied. There was a significant relationship between abnormal ventilation scans and abnormal results for PaO2 and end-tidal airflow. Bronchoscopy revealed excessive mucus and inflammation of airway mucosa in all 16 dogs undergoing this procedure. Endoscopically obtained aerobic bacterial cultures grew mixed bacterial flora in only three dogs. Increased numbers of neutrophils in 14 dogs were detected by airway lavage cytology. A large number of eosinophils were seen in airway lavages obtained from two dogs; these two dogs also had evidence for eosinophilic bronchitis on endobronchial biopsy. Oral bronchodilator administration resulted in clinical and expiratory airflow improvements in most dogs, but had no effect on PaO2 or on the radioaerosol-scan abnormalities. The presence of both the physiologic and pathologic airway abnormalities of chronic bronchitis in dogs presented to a veterinary hospital with chronic unexplained cough was confirmed, suggesting that aerobic bacteria do not play an etiologic role in most cases.

Albuterol↗