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)

DL50 of intraperitoneal lithium oxybutyrate administered to cats was found to amount to 724 mg/kg, while in doses of 13.5--360 mg/kg it increases the coronary blood flow volume in cats by 20.3--122.2 per cent, directly proportional to the dose. Lithium oxybutyrate prevents the chlorocalcium arrhythmia in rats and eliminates strophanthine-induced anemia in cats, surpassing an analogous effect of lithium chloride, potassium chloride, quinidine, novocainamide and isoptin. It raises the activity of the succinate dehydrogenase in the myocardium and weakens the ability of calcium chloride to reduce the glycogen content in the conduction system of the heart in rats.
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PMID:[Effect of lithium hydroxybutyrate on several heart function indices]. 42 89

Lithium and nickel present low toxicity, but are able to cause alterations in different tissues. The toxic effects of lithium and nickel at different cellular levels were assessed using two inorganic chemical species: lithium chloride and nickel(II) chloride. Mouse neuroblastoma cell cultures (Neuro-2a) were exposed to both compounds for 24 h. The cytotoxic effects evaluated were cell proliferation by quantification of total protein content, cytoplasmic membrane integrity to cytosolic lactate dehydrogenase leakage, and lysosomal hexosaminidase release. Metabolic markers were lactate dehydrogenase activity and mitochondrial succinate dehydrogenase activity. Lysosomal markers were relative neutral red uptake by lysosomes, and lysosomal hexosaminidase sphingolipid degradation activity. Acetylcholinesterase activity on intact cells was also quantified. Nickel was found to be 36 times more toxic than lithium to neuroblastoma cell proliferation (EC(50)= 0.29 and 10.5 mM, respectively), but the relative extent of other alterations differed. Lithium stimulated nearly all the indicators studied, particularly lactate dehydrogenase, mitochondrial succinate dehydrogenase and acetylcholinesterase activities, as well as hexosaminidase release. In contrast, nickel mainly stimulated hexosaminidase release and inhibited lactate dehydrogenase activity. The stabilization of the cytoplasmic membrane to lactate dehydrogenase leakage simultaneously with the secretion of lysosomal hexosaminidase for both compounds also shows that functional metabolic alterations produced by lithium and nickel are more important than cytoplasmic damage.
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PMID:In vitro effects of lithium and nickel at different levels on Neuro-2a mouse neuroblastoma cells. 1156 64