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

Neuronal activity and oxidative energy metabolism are tightly coupled. There is evidence that cytochrome oxidase, the terminal enzyme of the electron transport chain, can serve as a metabolic marker of neuronal activity. All the respiratory chain enzymes have iron containing prosthetic groups and therefore represent an important component of iron utilisation. Since iron entry into cells is mediated by the transferrin receptor, this receptor may also serve as marker of neuronal activity. The histochemical distribution of cytochrome oxidase has therefore been compared with the autoradiographic distribution of the transferrin receptor in the human spinal cord, brainstem and cerebellum. Cytochrome oxidase activity showed a very similar pattern of distribution to the transferrin receptor in the spinal cord, brainstem and cerebellum. The highest levels of cytochrome oxidase activity and transferrin receptor binding were associated with; in the spinal cord, the substantia gelatinosa, laminae II and III and the motor neurones; in the medulla and pons, the spinal trigeminal nucleus, hypoglossal nucleus, dorsal motor nucleus of the vagus, inferior and superior olives, nucleus praepositus, nucleus paramedianus, central grey, superior central nuclei and locus coeruleus; in the cerebellum, the molecular layer. The results suggest that the transferrin receptor may provide a useful marker of total neuronal respiratory activity.
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PMID:Distribution of transferrin receptors in relation to cytochrome oxidase activity in the human spinal cord, lower brainstem and cerebellum. 133 38

Cu and Fe metabolism are known to be linked, but the interactions during pregnancy are less well studied. In the present study we used rats to examine the effect of Cu deficiency during pregnancy on Fe and Cu levels in maternal and fetal tissue and on the gene expression profile of proteins involved in Cu and Fe metabolism in the placenta. Rats were fed diets with different Cu contents before and during pregnancy. Samples were collected on day 21 of gestation. Cu levels, ceruloplasmin activity and serum Fe all decreased in maternal serum of Cu-deficient animals. Maternal liver Fe inversely correlated with liver Cu. Placental Cu levels decreased with no change in Fe. Fe and Cu levels both decreased in the fetal liver. The drop in maternal liver Cu was significantly correlated with a decrease in organ weight of fetal liver, lung and kidney. No changes were observed in mRNA expression of Cu transporter 1, Menkes P-type Cu-ATPase 7A, Wilson P-type Cu-ATPase 7B, cytochrome-c oxidase, and Cu chaperone Atox1 in the placenta of Cu-deficient dams. Transferrin receptor 1 and the Fe-responsive element (IRE)-regulated divalent metal transporter 1 (DMT1) were up regulated; while ferroportin and non-IRE1-regulated DMT1 levels did not change. These data show that Cu deficiency during pregnancy not only has a direct effect on Fe levels but also regulates the expression of Fe transporters. The pattern closely mirrors that seen in Fe deficiency, suggesting that the changes are a consequence of the decrease in serum Fe, implying that the developing fetus not only suffers from Cu, but also from Fe deficiency.
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PMID:Effect of dietary copper deficiency on iron metabolism in the pregnant rat. 1729 91