Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In sheep from biogeochemical provinces enriched by molybdenum and copper and in a model form of molybdenum toxicosis in animals, the important role of enzymic and neurohumoral systems in the development of adaptation to excessive uptake of molybdenum and copper has been demonstrated. Adaptive reorganization of the activity of enzymic systems (xanthine oxidase, ceruloplasmin, succinate dehydrogenase, aspartate and alanine aminotransferases) and gradual involvement of neurohumoral mechanisms of the sympathoadrenal and cholinoreactive systems provide for adaptation of some animals in molybdenum and copper-molybdenum biogeochemical provinces. In other sheep, under the same conditions, dystonic disturbances in the vegetative nervous systems are observed together with the development of molybdenum toxicosis.
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PMID:[The enzymatic chemical mechanisms of adaptation]. 183 7

Intramuscular injections of the title drug in a dose of 5 mg/kg (5% of the LD50) during 10 days produced in the liver and blood serum of white rats a decrease in the activity of glucokinase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione reductase, ATPase and ceruloplasmin. The urea content in total phospholipids rose, whereas the content of triglycerides and hexosamine diminished. Ten and 20 days after the drug was discontinued the majority of these characteristics returned to normal. The activity of glucosophosphate isomerase, transketolase, glucose-6-phosphatase, fructose-1,6-diphosphatase and lactate dehydrogenase as well as the content of total cholesterol, free fatty acids, tyrosine, hydroxyproline, total protein, RNA and DNA remained unchanged.
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PMID:[Effect of decane-1,10-bis[acetoxy-(N, N)-dimethyl-(N)-(diphenylmethoxy-2-ethyl) ammonium] dichloride on metabolism in white rats]. 651 57

Age related mitochondrial impairments are considered to be contributors of cardiovascular disease. This study was designed to examine whether early life exposure to lead (Pb) would lead to the Pb induced age related hematological and cardiac mitochondrial changes in rats, and to further examine the protective effect of nutrient metal mixture containing zinc, iron and calcium. Male albino rats were lactationally exposed to 0.2 % Pb-acetate or 0.2 % Pb-acetate together nutrient metal mixture (0.02 %) in drinking water of the mother from postnatal day 1 (PND1) to PND 21. The hemoglobin level, the activities of serum ceruloplasmin oxidase, cardiac mitochondrial enzymes catalase, manganese superoxide dismutase, copper zinc superoxide dismutase, glutathione peroxidase, succinate dehydrogenase, lipid peroxidation and Pb levels were analyzed at PND 45, 12 and 24 months age. The hematological parameters, and the cardiac TCA cycle and antioxidant enzyme markers and lipid peroxidation levels were significantly altered following Pb exposure in young rats (PND 45). These Pb induced changes persisted, though at much lower level in the aged rats. The Pb levels in blood and heart were also significantly higher in PND 45 and remained at detectable levels in older rats. The nutrient metal mixture containing iron, calcium and zinc significantly reversed these changes in all the chosen markers except lipid peroxidation in which the reversal effect was not significant. These data are supportive of age-related cardiac mitochondrial impairments and further provide evidence for the protective efficacy of nutrient metal mixture against Pb-toxicity.
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PMID:Lead-induced cardiac and hematological alterations in aging Wistar male rats: alleviating effects of nutrient metal mixture. 2253 43