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)

In the present work, we described the perinatal changes in mitochondrial maturation that contribute to metabolic development in the rat kidney. We focused on cytochrome-c oxidase activity and gene expression from the last three days of gestation to one day after birth. The role of adrenal steroids in the development of cytochrome-c oxidase expression and of mitochondrial DNA content was also investigated by studying the effects of fetal adrenalectomy. During the perinatal period, the developmental pattern of the cytochrome-c oxidase enzymatic complex exhibited parallel increases in transcript levels, protein content and enzyme activity, suggesting a transcriptional regulation of this enzyme. Adrenalectomy led to a decrease in fetal kidney cytochrome-c oxidase messengers and mtDNA content while administration of dexamethasone restored normal levels. In contrast, mtDNA content was unchanged in liver and heart after adrenalectomy whereas levels of cytochrome-c oxidase transcripts were controlled by adrenal steroids in liver but not in heart. These results indicate that adrenal steroid hormones contribute to the regulation of perinatal maturation of mitochondria in rat kidney and that these hormones are involved in the fetal mitochondrial biogenesis in a tissue-specific manner.
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PMID:Effects of adrenal steroid hormones on mitochondrial maturation during the late fetal period. 952 88

Prenatal iron deficiency alters fetal developmental trajectories, which results in persistent changes in organ function. Here, we studied the effects of prenatal iron deficiency on fetal kidney and liver mitochondrial function. Pregnant Sprague-Dawley rats were fed partially or fully iron-restricted diets to induce a state of moderate or severe iron deficiency alongside iron-replete control rats. We assessed mitochondrial function via high-resolution respirometry and reactive oxygen species generation via fluorescence microscopy on gestational d 21. Hemoglobin levels were reduced in dams in the moderate (-31%) and severe groups (-54%) compared with controls, which was accompanied by 55% reductions in fetal hemoglobin levels in both moderate and severe groups versus controls. Male iron-deficient kidneys exhibited globally reduced mitochondrial content and respiration, as well as increased cytosolic superoxide and decreased NO. Female iron-deficient kidneys exhibited complex II down-regulation and increased mitochondrial oxidative stress. Male iron-deficient livers exhibited reduced complex IV respiration and increased cytosolic superoxide, whereas female liver tissues exhibited no alteration in oxidant levels or mitochondrial function. These findings indicate that prenatal iron deficiency causes changes in mitochondrial content and function as well as oxidant status in a sex- and organ-dependent manner, which may be an important mechanism that underlies the programming of cardiovascular disease.-Woodman, A. G., Mah, R., Keddie, D., Noble, R. M. N., Panahi, S., Gragasin, F. S., Lemieux, H., Bourque, S. L. Prenatal iron deficiency causes sex-dependent mitochondrial dysfunction and oxidative stress in fetal rat kidneys and liver.
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PMID:Prenatal iron deficiency causes sex-dependent mitochondrial dysfunction and oxidative stress in fetal rat kidneys and liver. 2940 11