Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.4.1.18 (branching enzyme)
 628 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific activities of the succinate dehydrogenase-coenzyme Q reductase were determined in mitochondria from the thymus and the spleen of aged mice (20, 22 and 24 months) as compared with young mice (10 weeks). Significant steep escalation of the deficiency of coenzyme Q-enzyme activity was observed in the thymus of all three groups of aged mice. No significant deficiency was found in the mitochondria of the spleen. The ratios between the liver weight:body weight and the spleen weight:body weight in young and aged mice are practically unchanged, but the thymus weight:body weight ratio decreases significantly in all three groups of aged mice. The described age-dependent anatomical and functional alterations in the thymus most likely form the base for the development of the T cell determined suppression of the immunological responsiveness, present in aged mice.
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PMID:Coenzyme Q deficiency in aged mice. 28 77

The specific activities of the succinate dehydrogenase-coenzyme Q reductase were assayed on mitochondrial preparations of this enzyme from spleen, liver, blood and peritoneal macrophages of mice infected with Friend leukemia virus, and of control mice. Significant increases in the deficiency of coenzyme Q-enzyme activity were found in the spleen and blood of infected animals as the infection progressed. No significant deficiency was observed in the liver or the peritoneal macrophages. The development of the deficiency and splenomegaly during infection seemingly correlate with previous data which showed that administration of coenzyme Q resulted in a reversal of splenomegaly and a reduction in mortality. A limiting factor in the resistance of mice to Friend leukemia virus appears to be the availability of coenzyme Q.
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PMID:Coenzyme Q deficiency in mice following infection with Friend leukemia virus. 121 65

Although arterial limb tourniquet is one of the first-line treatments to prevent exsanguinating hemorrhage in both civilian pre-hospital and battlefield casualty care, prolonged application of a limb tourniquet can lead to serious ischemia-reperfusion injury. However, the underlying pathomechanisms of tourniquet-induced ischemia-reperfusion injury are still poorly understood. Using a murine model of acute limb ischemia-reperfusion, we investigated if acute limb ischemia-reperfusion injury is mediated by superoxide overproduction and mitochondrial dysfunction. Hind limbs of C57/BL6 mice were subjected to 3h ischemia and 4h reperfusion via placement and release of a rubber tourniquet at the greater trochanter. Approximately 40% of the gastrocnemius muscle suffered infarction in this model. Activities of mitochondrial electron transport chain complexes including complex I, II, III, and IV in the gastrocnemius muscle were decreased in the ischemia-reperfusion group compared to sham. Superoxide production was increased while activity of manganese superoxide dismutase (MnSOD, the mitochondria-targeted SOD isoform) was decreased in the ischemia-reperfusion group compared to the sham group. Pretreatment with tempol (a SOD mimetic, 50mg/kg) or co-enzyme Q(10) (50mg/kg) not only decreased the superoxide production, but also reduced the infarct size and normalized mitochondrial dysfunction in the gastrocnemius muscle. Our results suggest that tourniquet-induced skeletal muscle ischemia-reperfusion injuries including infarct size and mitochondrial dysfunction may be mediated via superoxide overproduction and reduced antioxidant activity. In the future, this murine ischemia-reperfusion model can be adapted to mechanistically evaluate anti-ischemic molecules in tourniquet-induced skeletal muscle injury.
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PMID:Tourniquet-induced acute ischemia-reperfusion injury in mouse skeletal muscles: Involvement of superoxide. 2103 24