Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spermine activated citrate synthase from porcine heart by decreasing the Km value for the substrate oxaloacetate without affecting the maximal velocity. Spermine markedly increased the maximal velocity of the saturation function with respect to acetyl-CoA as the substrate under conditions of intracellular concentrations of oxaloacetate, but the enzyme was not activated by spermine under conditions of higher concentrations of oxaloacetate. The concentration of spermine required for 50% activation of the enzyme was about 50 microM. Spermidine showed only a little activation, while putrescine caused no activation. Spermine, which contributes to an activation of Ca2(+)-sensitive dehydrogenases of the citric acid cycle by enhancing Ca2+ uptake into mitochondria, can activate citrate synthase directly, and is responsible for the stimulation of oxidative metabolism in mitochondria.
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PMID:Activation by spermine of citrate synthase from porcine heart. 199 Nov 36

The polyamines (spermine, putrescine, and spermidine) can have neurotoxic or neuroprotective properties in models of neurodegeneration. However, assessment in a model of hypoxia-ischemia (HI) has not been defined. Furthermore, the putative mechanisms of neuroprotection have not been elucidated. Therefore, the present study examined the effects of the polyamines in a rat pup model of HI and determined effects on key enzymes involved in inflammation, namely, nitric oxide synthase (NOS) and arginase. In addition, effects on mitochondrial function were investigated. The polyamines or saline were administered i.p. at 10mg/kg/day for 6 days post-HI. Histological assessment 7 days post-HI revealed that only spermine significantly (P<0.01) reduced infarct size from 46.14 +/- 10.4 mm3 (HI + saline) to 4.9 +/- 2.7 mm3. NOS activity was significantly increased following spermine treatment in the left (ligated) hemisphere compared with nonintervention controls (P<0.01) and HI + saline (P<0.05). In contrast, spermine decreased arginase activity compared with HI + saline but was still significantly elevated in comparison to nonintervention controls (P<0.01). Assessment of mitochondrial function in the HI + saline group, revealed significant and extensive damage to complex-I (P<0.01) and IV (P<0.001) and loss of citrate synthase activity (P<0.05). No effect on complex II-III was observed. Spermine treatment significantly prevented all these effects. This study has therefore confirmed the neuroprotective effects of spermine in vivo. However, for the first time, we have shown that this effect may, in part, be due to increased NOS activity and preservation of mitochondrial function.
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PMID:Neuroprotective effects of spermine following hypoxic-ischemic-induced brain damage: a mechanistic study. 1513 86