Creatine kinase in serum: 1. Determination of optimum reaction conditions.

Szasz, G; Gruber, Wolfgang; Bernt, Erich

doi:10.1093/clinchem/22.5.650

Cited by 407 publications

(100 citation statements)

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“…Detailed histological images depicting muscle necrosis in the model used in the present study were presented in Westwood et al (2005). Plasma CK concentration (IU l −1 ) was also determined using a spectrophotometric assay (Szasz et al 1976).…”

Section: Quantification Of Muscle Necrosismentioning

confidence: 99%

Pharmacological activation of the pyruvate dehydrogenase complex reduces statin‐mediated upregulation of FOXO gene targets and protects against statin myopathy in rodents

Mallinson

Constantin‐Teodosiu

Glaves

et al. 2012

The Journal of Physiology

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Key points• Statin myopathy impairs phosphatidylinositol 3-kinase/Akt signalling and activates forkhead box protein O (FOXO) transcription factors in vivo in rodent skeletal muscle. This is associated with upregulation of downstream gene targets known to increase proteasomal and lysosomal-mediated protein breakdown, oxidative stress and inflammation, and inhibit muscle carbohydrate (CHO) oxidation.• We hypothesised that forcibly increasing muscle CHO oxidation in vivo, using the pyruvate dehydrogenase complex activator, dichloroacetate (DCA), would blunt statin-mediated increases in mRNA expression of these FOXO gene targets, thereby reducing statin myopathy.• Chronic administration of DCA with simvastatin dampened statin-mediated increases in muscle atrophy F-box (MAFbx), cathepsin-L and pyruvate dehydrogenase kinase-4 mRNA in a dose-dependent manner, which was corroborated by protein activity and expression measurements, and blunted statin myopathy.• These results provide convincing evidence that pharmacologically increasing muscle CHO oxidation reduces simvastatin-induced myopathy by dampening the upregulation of genes known to increase proteasomal and lysosomal protein breakdown and inhibit CHO oxidation.Abstract We previously reported that statin myopathy is associated with impaired carbohydrate (CHO) oxidation in fast-twitch rodent skeletal muscle, which we hypothesised occurred as a result of forkhead box protein O1 (FOXO1) mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) gene transcription. Upregulation of FOXO gene targets known to regulate proteasomal and lysosomal muscle protein breakdown was also evident. We hypothesised that increasing CHO oxidation in vivo, using the pyruvate dehydrogenase complex (PDC) activator, dichloroacetate (DCA), would blunt activation of FOXO gene targets and reduce statin myopathy. Female Wistar Hanover rats were dosed daily for 12 days (oral gavage) with either vehicle (control, 0.5% w/v hydroxypropyl-methylcellulose 0.1% w/v polysorbate-80; n = 9), 88 mg kg −1 day −1 simvastatin (n = 8), 88 mg kg −1 day −1 simvastatin + 30 mg kg −1 day −1 DCA (n = 9) or 88 mg kg −1 day −1 simvastatin + 40 mg kg −1 day −1 DCA (n = 9). Compared with control, simvastatin reduced body mass gain and food intake, increased muscle fibre necrosis, plasma creatine kinase levels, muscle PDK4, muscle atrophy F-box (MAFbx) and cathepsin-L mRNA expression, increased PDK4 protein expression, and proteasome and cathepsin-L activity, and reduced muscle PDC activity. Simvastatin with DCA maintained body mass gain and food intake, abrogated the myopathy, decreased muscle PDK4 mRNA and protein, MAFbx and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvastatin. PDC activation abolished statin myopathy in rodent skeletal muscle, which occurred at least in part via inhibition of FOXO-mediated transcription of genes regulating muscle CHO utilisation and protein breakdown.

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Section: Quantification Of Muscle Necrosismentioning

confidence: 99%

Pharmacological activation of the pyruvate dehydrogenase complex reduces statin‐mediated upregulation of FOXO gene targets and protects against statin myopathy in rodents

Mallinson

Constantin‐Teodosiu

Glaves

et al. 2012

The Journal of Physiology

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“…LDH was measured according to Bergmeyer and Bernt (1974) using kits from the Human Gesellschaft fuÈ r Biochemica und Diagnostica mbH, Germany. CK was measured according to Szasz et al (1976) by clinical kits from the Human Gesellschaft fuÈ r Biochemica and Diagnostica mbH, Germany. ChE was determined according to Weber (1966) using standard kits (Test-combination Boehringer Mannheim GmbH Diagnostica).…”

Section: Colorimetric Determinations Of Blood Serummentioning

confidence: 99%

Sublethal effects of aquatic pollution in Lake Maryut on the African sharptooth catfish, Clarias gariepinus (Burchell, 1822)

Adham

2002

J Appl Ichthyol

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Some aspects of the physiology and biochemistry of the African sharptooth catfish, Clarias gariepinus (Burchell, 1822), were studied along with an array of physicochemical characteristics of the water in Lake Maryût, Egypt. Data were compared to those of a reference fish hatchery. At least 11 of the conventional water pollutants (Cd, Cu, Fe, Pb, Mn, Hg, Ni, Zn, turbidity, chemical oxygen demand and ammonia nitrogen) were elevated in the most polluted main basin of the lake. In turn, serologic analysis of the indigenous catfish C. gariepinus pointed at functional impairment of the liver, heart and kidney as reflected by the elevated activities of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, creatine kinase, cholinesterase, glucose and creatinine. Reduced nucleic acid measurements [the ratio RNA/DNA and the relative RNA content (r)] indicated diminished protein synthesis and impaired growth in polluted fish. In some instances, glucose and nucleic acid measures were elevated in favour of fish from moderately polluted basins of the lake rather than in reference fish. Fish seemed to profit from the typical geographical habitat in the lake, regardless of the virtual contamination there, versus reference fish that seemed to suffer congestion stress and food competition in the confined and overcrowded commercial pond.

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“…The state of differentiation into myotubes (SKMmt) was monitored by the appearance of multinucleated cells, assessed by light microscopy following nuclear staining with propidium iodide. The activities of two marker enzymes of differentiation, creatine kinase (CK) (22) and citrate synthetase (CS) (23), were monitored before and after the differentiation period, as described below.…”

Section: Myoblast Culture and Differentiationmentioning

confidence: 99%

“…The activities of CK (22) and citrate synthetase (CS) (23) were assayed in cellular extracts of SKMmbs and SKMmts, as previously described.…”

Section: Enzyme Assaysmentioning

confidence: 99%

Differentiation‐specific alterations to glutathione synthesis in hormonally stimulated release from human skeletal muscle cells

et al. 2002

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Muscle atrophy and cachexia are associated with many human diseases. These catabolic states are often associated with the loss of glutathione (GSH), which is thought to contribute to the induction of oxidative stress within the muscle. Glutathione synthesis and secretary characteristics were studied in human skeletal muscle myoblasts and myotube-like cells derived from the myoblasts by growth factor restriction. Differentiation was associated with a shift in the sulfur amino acid precursor specificity for synthesis of GSH from cystine to cysteine, as well as loss in ability to use extracellular glutathione and activation of methionine use. The thiol drug N-acetylcysteine was also shown to be an effective precursor irrespective of the state of differentiation. Additionally, myoblasts and myotube cultures were shown to secrete GSH continually, but only the differentiated cells responded to stress hormones such as glucagon, vasopressin, and phenylephrine, by increased secretion of the tripeptide. The data suggest that the skeletal muscle cells may provide an important hormonally regulated extra-hepatic source of systemic GSH and also shed light on the mechanisms of accelerated turnover of GSH operating during strenuous muscle activity and trauma. The data may also provide biochemical rationales for the nutritional and/or pharmacological manipulation of GSH with sulfur amino acid precursors during the treatment of muscle-specific oxidative stress and atrophy.

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Creatine kinase in serum: 1. Determination of optimum reaction conditions.

Cited by 407 publications

References 0 publications

Pharmacological activation of the pyruvate dehydrogenase complex reduces statin‐mediated upregulation of FOXO gene targets and protects against statin myopathy in rodents

Pharmacological activation of the pyruvate dehydrogenase complex reduces statin‐mediated upregulation of FOXO gene targets and protects against statin myopathy in rodents

Sublethal effects of aquatic pollution in Lake Maryut on the African sharptooth catfish, Clarias gariepinus (Burchell, 1822)

Differentiation‐specific alterations to glutathione synthesis in hormonally stimulated release from human skeletal muscle cells

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