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)

The middle portion of Meckel's cartilage resembles endochondral bone formation accompanied by chondrocyte hypertrophy and death, cartilaginous matrix calcification, and chondroclastic resorption. We examined Meckel's cartilage specimens from mice mandibles taken on embryonic days 14-16 (E14-E16) using immunohistochemistry for hypoxia-inducible factor-1alpha (HIF-1alpha), glucose transporter 1 (GLUT1), glucose transporter 3 (GLUT3), and glucose transporter 5 (GLUT5), and using enzyme histochemistry for glucose-6-phosphate isomerase (GPI), lactate dehydrogenase (LDH), and cytochrome oxidase (COX), along with the periodic acid-Schiff (PAS) reaction, and compared the results with those of endochondral bones from E16 hind limbs. Periodic acid-Schiff-positive glycogen, HIF-1alpha, and GLUT immunoreactivity, and GPI, LDH, and COX activities were observed in Meckel's cartilage in E14 and E15 mandibles. In E16 mandibles, hypertrophic chondrocytes showed a transitory loss of HIF-1alpha immunoreactivity and consumed glycogen, while those closest to the resorption front showed intense immunoreactivity for HIF-1, GLUT3, and GLUT5. Hypertrophic chondrocytes of metatarsals possessed HIF-1alpha immunoreactivity in the nuclei and diminished COX activity, whereas developing tibias showed weak HIF-1alpha immunoreactivity even in hypoxic regions characterized by little or no COX activity. These findings suggest that HIF-1alpha becomes stabilized independently of the concentration of oxygen, and largely contributes to the development and resorption of Meckel's cartilage, probably through shifting the predominant metabolic mode from aerobic to anaerobic glycolysis.
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PMID:Metabolic mode peculiar to Meckel's cartilage: immunohistochemical comparisons of hypoxia-inducible factor-1alpha and glucose transporters in developing endochondral bones in mice. 1870 2

The dmy rat is an autosomal recessive mutant that exhibits severe myelin destruction throughout the white matter of the central nervous system. Recently, a point mutation in intron 3 of the Mrs2 has been found in the dmy rat. Mrs2 encodes an essential component of the major electrophoretic Mg(2+) influx system in mitochondria of yeast as well as human cells. In this study, we examined the morphological and numerical changes of oligodendroctyes in the development of myelin destruction in the spinal cord of the dmy rat. The number of oligodendrocytes decreases rapidly from 7weeks of age in the dmy rat in accordance with myelin breakdown. Hypertrophic oligodendrocytes were frequently observed, and the cytoplasm was found to be intensely positive for prohibitin and cytochrome oxidase, mitochondrial markers. These data suggest that mitochondrial dysfunction causes a work/compensatory hypertrophy of oligodendrocytes, resulting in direct cell death and leading to myelin destruction.
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PMID:Oligodendroglial pathology in the development of myelin breakdown in the dmy mutant rat. 2139 20