Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.9.3.1 (
cytochrome oxidase
)
8,822
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Reactive oxygen species may contribute to the pathogenesis of muscular dystrophy. High intensity exercise clearly induces muscle damage in mdx mice; however, the effects of low intensity exercise training (LIT) on mdx muscle are less clear. We examined the effect of LIT on markers of oxidative stress (malondialdehyde and protein carbonyls), antioxidant (superoxide dismutase, catalase, and glutathione peroxidase), and mitochondrial (2-oxoglutarate dehydrogenase and
cytochrome oxidase
) enzymes in skeletal muscle of mdx and wild-type mice. Mdx and wild-type mice were allocated to LIT and sedentary groups.
Malondialdehyde
levels were higher in white muscle from sedentary mdx as compared to both sedentary and LIT wild-type mice (P<0.001). Protein carbonyl content was higher in white and red muscle of mdx versus wild-type mice (P<0.05). LIT was associated with lower levels of malondialdehyde and protein carbonyls in white muscle of mdx mice (decreased 38 and 44%, P<0.001 and P<0.01, respectively). Antioxidant and mitochondrial enzyme activities were higher in white muscle of mdx than in wild-type mice (P<0.05). LIT in mdx mice induced physiological adaptation resulting in lower levels of markers of oxidative stress that were not different than those from wild type. These results are of relevance for therapeutic exercise in patients with dystrophinopathy where exercise prescription remains controversial.
...
PMID:Low intensity training decreases markers of oxidative stress in skeletal muscle of mdx mice. 1756 Nov 3
Oophorectomy in adult rats affected cardiac mitochondrial function. Progression of mitochondrial alterations was assessed at one, two and three months after surgery: at one month, very slight changes were observed, which increased at two and three months. Gradual effects included decrease in the rates of oxygen consumption and in respiratory uncoupling in the presence of complex I substrates, as well as compromised Ca
2+
buffering ability.
Malondialdehyde
concentration increased, whereas the ROS-detoxifying enzyme Mn
2+
superoxide dismutase (MnSOD) and aconitase lost activity. In the mitochondrial respiratory chain, the concentration and activity of complex I and
complex IV
decreased. Among other mitochondrial enzymes and transporters, adenine nucleotide carrier and glutaminase decreased. 2-Oxoglutarate dehydrogenase and pyruvate dehydrogenase also decreased. Data strongly suggest that in the female rat heart, estrogen depletion leads to progressive, severe mitochondrial dysfunction.
...
PMID:In female rat heart mitochondria, oophorectomy results in loss of oxidative phosphorylation. 2787 98
