Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sojourns to high altitude have become common for recreation and adventure purposes. In most individuals, gradual ascent to a high altitude leads to a series of adaptive changes in the body, termed as acclimatization. These include changes in the respiratory, cardiovascular, hematologic systems and cellular adaptations that enhance oxygen delivery to the tissues and augment oxygen uptake. Thus there is an increase in pulmonary ventilation, increase in diffusing capacity in the lung, an increase in the cardiac output and increase in the red blood cell count due to an increase in erythropoietin secretion by the kidney, all of which enhance oxygen delivery to the cells. Cellular changes like increase in the number of mitochondria and augmentation of cytochrome oxidase systems take months or years to develop. Too rapid an ascent or inability to acclimatize leads to high-altitude illnesses. These include acute mountain sickness (AMS), high-altitude cerebral edema (HACE) and high-altitude pulmonary edema (HAPE). Acute mountain sickness is self limiting if recognized early. Both HACE and HAPE are life threatening and need to be treated aggressively. The key to treatment of these illnesses is early recognition; administration of supplemental oxygen; and descent if required. Drugs like acetazolamide, dexamethasone, nifedipine may be administered as recommended.
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PMID:High-altitude medicine. 2080 61

Compared with mice, adult rats living at 3,600 m above sea level (SL-La Paz, Bolivia) have high hematocrit, signs of pulmonary hypertension, and low lung volume with reduced alveolar surface area. This phenotype is associated with chronic mountain sickness in humans living at high altitude (HA). We tested the hypothesis that this phenotype is associated with impaired gas exchange and oxidative stress in the lungs. We used rats and mice (3 months old) living at HA (La Paz) and SL (Quebec City, Canada) to measure arterial oxygen saturation under graded levels of hypoxia (by pulse oximetry), the alveolar surface area in lung slices and the activity of pro- (NADPH and xanthine oxidases-NOX and XO) and anti- (superoxide dismutase, and glutathione peroxidase-SOD and GPx) oxidant enzymes in cytosolic and mitochondrial lung protein extracts. HA rats have a lower arterial oxygen saturation and reduced alveolar surface area compared to HA mice and SL rats. Enzymatic activities (NOX, XO, SOD, and GPx) in the cytosol were similar between HA and SL animals, but SOD and GPx activities in the mitochondria were 2-3 times higher in HA vs. SL rats, and only marginally higher in HA mice vs. SL mice. Furthermore, the maximum activity of cytochrome oxidase-c (COX) measured in mitochondrial lung extracts was also 2 times higher in HA rats compared with SL rats, while there was only a small increase in HA mice vs. SL mice. Interestingly, compared with SL controls, alterations in lung morphology are not observed for young rats at HA (15 days after birth), and enzymatic activities are only slightly altered. These results suggest that rats living at HA have a gradual reduction of their alveolar surface area beyond the postnatal period. We can speculate that the elevation of SOD, GPx, and COX activities in the lung mitochondria are not sufficient to compensate for oxidative stress, leading to damage of the lung tissue in rats.
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PMID:Divergent Mitochondrial Antioxidant Activities and Lung Alveolar Architecture in the Lungs of Rats and Mice at High Altitude. 2967 May 34