Regulation of mitochondrial NADP-isocitrate dehydrogenase in rat heart during ischemia

Попова, Т. Н.; Carvalho, M. A. A. Pinheiro de; Matasova, L. V.; Medvedeva, L.V.

doi:10.1007/s11010-006-9249-9

Cited by 11 publications

(7 citation statements)

References 46 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Citrate is a known inhibitor of many central metabolic enzymes, including 6-phosphofructokinase (K d = 20 mM; Newsholme et al, 1977;Ogawa & Atkinson, 1985;Colombo et al, 1975) and isocitrate dehydrogenase (K i = 160 mM; Popova et al, 2007). It is also an effective inhibitor of members of the acid phosphatase superfamily, including 6-phosphofructo-2-kinase (K i = 35 mM for kinase activity; Ventura et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Unliganded structure of human bisphosphoglycerate mutase reveals side-chain movements induced by ligand binding

2010

View full text Add to dashboard Cite

PDB Reference: bisphosphoglycerate mutase, 3nfy.Erythrocyte-specific bisphosphoglycerate mutase is a trifunctional enzyme which modulates the levels of 2,3-bisphosphoglycerate (2,3-BPG) in red blood cells by virtue of its synthase and phosphatase activities. Low levels of erythrocyte 2,3-BPG increase the affinity of haemoglobin for oxygen, thus limiting the release of oxygen into tissues. 2,3-BPG levels in stored blood decline rapidly owing to the phosphatase activity of bisphosphoglycerate mutase, which is enhanced by a fall in pH. Here, the 1.94 Å resolution X-ray structure of bisphosphoglycerate mutase is presented, focusing on the dynamic nature of key ligand-binding residues and their interaction with the inhibitor citrate. Residues at the binding pocket are complete. In addition, the movement of key residues in the presence and absence of ligand is described and alternative conformations are explored. The conformation in which the ligand citrate would bind at the substrate-binding pocket is proposed, with discussion and representations of its orientation. The characterization of bisphosphoglycerate mutase-citrate interactions will provide a framework for the design of specific inhibitors of the phosphatase activity of this enzyme, which may limit the decline of 2,3-BPG in stored blood.

show abstract

Section: Discussionmentioning

confidence: 99%

Unliganded structure of human bisphosphoglycerate mutase reveals side-chain movements induced by ligand binding

2010

View full text Add to dashboard Cite

show abstract

“…Mitochondrial glutathione reductase (GRD) and Se-glutathione peroxidise (GPX) activities were measured as described by Chiu et al [28]. Mitochondrial isocitrate dehydrogenase (ICDH) activity was measured according to the method by Popova et al [29]. Plasma and mitochondrial parameters were expressed as the percentage of control ( ie basal value in saline injected animals).…”

Section: Methodsmentioning

confidence: 99%

Myocardial post-conditioning with Danshen-Gegen decoction protects against isoproterenol-induced myocardial injury via a PKCε/mKATP-mediated pathway in rats

et al. 2011

View full text Add to dashboard Cite

Background: Danshen-Gegen decoction (DG), a Chinese herbal formula, has been demonstrated to be effective for the treatment of coronary heart disease such as myocardial infarction. In the present study, we investigated the effect of DG post-conditioning on isoproterenol (ISO)-induced myocardial injury in rats. Methods: ISO was injected intraperitoneally (200 mg/kg) to induce acute (2-6 hours) myocardial injury in adult female rats. DG (4 g/kg) was administered per oral immediately after the injection of ISO in the rats. Extent of myocardial injury was assessed by measurements of plasma enzyme activities. Myocardial mitochondrial glutathione antioxidant status, lipid peroxidation and mitochondrial calcium ion loading and cytochrome c release were also measured. Effects of inhibitors of protein kinase C-epsilon (PKCε) ranslocation and mitochondrial ATP-sensitive potassium channel (mK ATP ) on myocardial post-conditioning by DG were investigated. Results: ISO inflicted acute myocardial injury in the rats as evidenced by increased plasma enzyme activities. DG post-treatment alleviated the ISO-induced acute myocardial injury.

show abstract

“…To determine the activity of isocitrate dehydrogenase (ICDH), we used a reaction solution of 0.05 M Tris-HCl (pH 7.4), 0.2 mM MnCl 2 , 0.4 mM NADP, and 0.05 mM sodium isocitrate [ 46 ]; the activity of aconitase was determined in 0.1 M Tris-HCl (pH 7.4), 0.6 mM MnCl 2 , 0.2 mM NADP, 1.0 mM sodium citrate, and 1.0 U isocitrate dehydrogenase [ 47 ]. The change in absorbance at 340 nm was determined, and the activity of ICDH and aconitase was calculated using a molar extinction coefficient of 6.22 mM −1 cm −1 .…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of D-Panthenol in Rhabdomyolysis-Induced Acute Kidney Injury

Семенович

Plotnikov

Lukiyenko³

et al. 2022

IJMS

View full text Add to dashboard Cite

We investigated the nephroprotective effect of D-panthenol in rhabdomyolysis-induced acute kidney injury (AKI). Adult male Wistar rats were injected with 50% glycerol solution to induce rhabdomyolysis. Animals with rhabdomyolysis were injected with D-panthenol (200 mg/kg) for 7 days. On day 8, we examined AKI markers, renal histology, antioxidant capacity, and protein glutathionylation in kidneys to uncover mechanisms of D-panthenol effects. Rhabdomyolysis kidneys were shown to have pathomorphological alterations (mononuclear infiltration, dilatation of tubules, and hyaline casts in Henle’s loops and collecting ducts). Activities of skeletal muscle damage markers (creatine kinase and lactate dehydrogenase) increased, myoglobinuria was observed, and creatinine, BUN, and pantetheinase activity in serum and urine rose. Signs of oxidative stress in the kidney tissue of rhabdomyolysis rats, increased levels of lipid peroxidation products, and activities of antioxidant enzymes (SOD, catalase, and glutathione peroxidase) were all alleviated by administration of D-panthenol. Its application improved kidney morphology and decreased AKI markers. Mechanisms of D-panthenol’s beneficial effects were associated with an increase in total coenzyme A levels, activity of Krebs cycle enzymes, and attenuation of protein glutathionylation. D-Panthenol protects kidneys from rhabdomyolysis-induced AKI through antioxidant effects, normalization of mitochondrial metabolism, and modulation of glutathione-dependent signaling.

show abstract

Regulation of mitochondrial NADP-isocitrate dehydrogenase in rat heart during ischemia

Cited by 11 publications

References 46 publications

Unliganded structure of human bisphosphoglycerate mutase reveals side-chain movements induced by ligand binding

Unliganded structure of human bisphosphoglycerate mutase reveals side-chain movements induced by ligand binding

Myocardial post-conditioning with Danshen-Gegen decoction protects against isoproterenol-induced myocardial injury via a PKCε/mKATP-mediated pathway in rats

Protective Effect of D-Panthenol in Rhabdomyolysis-Induced Acute Kidney Injury

Contact Info

Product

Resources

About