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PubMed2001

Aggregation of creatine kinase during refolding and chaperonin-mediated folding of creatine kinase.

The course of refolding and reactivation of urea-denatured creatine kinase (ATP; creatine N-phosphotransferase, EC 2.7.3.2) has been studied in the absence and presence of molecular chaperonin GroEL. The enzyme was denatured in Tris--HCl buffer containing 6 M urea for 1 h. In the refolding studies, the denatured enzyme was diluted 60-fold into the same buffer containing GroEL or not for activity, turbidity, fluorescence measurements and polyacrylamide gel electrophoresis. The results show that the reactivation process is dependent of creatine kinase concentration in the concentration range 2.5--4 microM. The levels of activity recovery decrease with increasing enzyme concentration because of the formation of wrong aggregates. The molecular chaperonin GroEL can bind the refolding intermediate of creatine kinase and thus prevent the formation of wrong aggregates. This intermediate is an inactive dimeric form that is in a conformation resembling the 'molten globule' state.

Animals↗

PubMed2004

Elevation of creatine in red blood cells in vegetarians and nonvegetarians after creatine supplementation.

The purpose of this study was to examine the effect of a 5-day creatine (CR) supplementation period on red blood cell (RBC) CR uptake in vegetarian and nonvegetarian young women. Blood samples were collected from lacto-ovo vegetarians (VG, n = 6, age 21.8 +/- 1.9 yrs) and nonvegetarians (NV, n = 6, age 21.7 +/- 1.9 yrs) before and after a 5-day CR loading period (0. 3g CR/kg lean body mass/day), and from a control group of nonvegetarians (NV, n = 5, age 22.0 +/- 0.7 yrs) who did not supplement with creatine. RBC and plasma samples were analyzed for the presence of creatine. Significant increases (p < .05) in RBC and plasma CR levels were found for vegetarians and nonvegetarians following supplementation. The initial RBC CR content was significantly lower (p < .05) in the vegetarian group. There was no significant difference between vegetarians and nonvegetarians in final RBC CR content, suggesting that a ceiling had been reached. As the uptake into both muscle and RBC is moderated by creatine transporter proteins, analysis of the uptake of CR into RBC may reflect the uptake of CR into muscle, offering an alternative to biopsies.

Biopsy↗

PubMed1990

Myocardial adaptation to creatine deficiency in rats fed with beta-guanidinopropionic acid, a creatine analogue.

A creatine analogue, beta-guanidinopropionic acid (GPA), was fed to 12 young rats for several weeks. Another 12 animals were kept in the same conditions and age matched. Six pairs of animals were used to measure some energetic and mechanical parameters of the isovolumic perfused heart and to measure the accumulation of the phosphorylated form of GPA (GPAP) by 31P-nuclear magnetic resonance (NMR) spectroscopy. As a result of GPAP accumulation, phosphocreatine and ATP content decreased by 90 and 40%, respectively, and mechanical performance was impaired. Six other pairs of animals were used to assess the mechanical performances of Triton X-100-skinned fibers and the myosin isoenzyme distribution. It was found that the maximal force, Ca and ATP sensitivities, and myofibrillar creatine kinase efficacy of creatine-depleted hearts were similar to control values. There was, however, a decrease in the rate of cross-bridge cycling, and the isoenzymic expression of myosin was changed from the fast myosin V1 to the slower forms V2 and V3. In all animals, hypertrophy was observed in both right and left ventricles. We conclude that rat hearts subjected to a slow and persistent decrease in creatine and phosphocreatine respond with both quantitative and qualitative changes. These alterations, which most probably lead to an improvement in the economy of cardiac contraction, are nonetheless not sufficient to maintain maximal force.

Adaptation, Physiological↗

PubMed1999

Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance.

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 x (5 g Cr-H(2)O + 5 g dextrose)/day)] or a placebo (6 x 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased (P < 0.05) at 0 [by 22.9 +/- 4.2, 8.9 +/- 1.9, and 14.0 +/- 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.

Adolescent↗

PubMed1981

Macro creatine kinase BB: evidence for specific binding between creatine kinase BB and immunoglobulin G.

In the sera of four female patients with proven IgG-linked creatine kinase BB (macro creatine kinase BB) we studied the nature of the binding between creatine kinase isoenzymes and immunoglobulin G. The specificity towards the isoenzyme bound, the recombination of the complex after treatment with acid buffer, the site of the binding between both partners and an apparently monoclonal nature of the immunoglobulin G involved in the complex indicate that a specific antigen-antibody reaction is responsible for the existence of macro creatine kinase BB in the sera investigated.

Antigen-Antibody Complex↗

PubMed2000

Reversible brain creatine deficiency in two sisters with normal blood creatine level.

We describe a new creatine metabolism disorder in 2 young sisters who suffered from mental retardation and severe language delay. Blood examination, investigation of the most common neurometabolic disorders, and brain magnetic resonance imaging were normal. Diagnosis was established only by means of in vivo proton magnetic resonance spectroscopy, which disclosed generalized depletion of creatine in the brain. Creatine monohydrate oral administration led to almost complete brain creatine level restoration along with improvement of the patients' disabilities.

Brain Chemistry↗

PubMedDate not supplied

[Effect of vitamin E deficiency on creatine phosphokinase activity and creatine phosphate levels in the heart muscle].

Vitamin E deficient diet of rats developed impairments in energy metabolism of myocardium, involving a decrease in content of creatine phosphate and in the activity of creatine phosphokinase by 20-35%. Concentration of adenine nucleotides was not altered in myocardium and the content of glycogen was only slightly changed. The impairments in activity of creatine phosphokinase and in the content of creatine phosphate might be among the factors responsible for deterioration of the heart muscle contractile functions in avitaminosis E.

Animals↗

PubMed1984

Myoglobin concentration, creatine kinase activity, and creatine kinase B subunit concentrations in serum during thyroid disease.

Changes in values for myoglobin, total creatine kinase (EC 2.7.3.2), and creatine kinase B-subunit in the serum of patients with thyroid disease are compared with values for these during the 24-h after myocardial infarction. Concentrations of all three of these muscle-derived proteins were significantly higher than normal in patients with primary hypothyroidism, and declined with treatment. Values for total creatine kinase activity were below-normal in hyperthyroid patients, but increased after treatment. Values for total creatine kinase and, to a lesser extent, myoglobin in hypothyroidism extend into the range of values observed after myocardial infarction. The mechanism of the changes in these analytes in hypothyroidism may be related to increased leakage from skeletal-muscle cells or diminished clearance from the circulation, or both.

Creatine Kinase↗

PubMed1980

Metastable creatine kinase MM and complexes of creatine kinase BB and immunoglobulin G, "atypical" isoenzymes with similar electrophoretic mobility.

Metastable creatine kinase MM isoenzyme was isolated and partially purified from homogenates of myocardium and skeletal muscle by gradient elution on carboxymethyl cellulose. This variant isoenzyme migrated between the MM and MB isoenzymes on agarose electrophoresis, accounted for 3.5% of the total creatine kinase activity in each tissue, was not a macromolecule, and had stable electrophoretic mobility only in borate buffer (0.02 mol/L). By comparison, the creatine kinase isoenzymes with similar "atypical" electrophoretic mobility in serum specimens were complexes of the BB isoenzyme and immunoglobulin G. These complexes were measured by a radioimmunoassay specific for the creatine kinase B-subunit and eluted predominantly with the MB isoenzyme in a commercial anion-exchange reagent system.

Creatine Kinase↗

PubMed1996

[Measurements of serum activity of creatine kinase and creatine kinase isoenzyme MB in suspected myocardial infarction. Experiences from a hospital material].

Total creatine kinase and the creatine kinase isoenzyme MB activities were measured simultaneously in 767 serum samples from 592 patients with suspected myocardial infarction. The main and obligate finding was that in the 89 patients with verified infarction the fraction of MB-activity related to the total creatine kinase activity lay between 4 and 25%. In 72 patients diagnosed as not-having an infarction this fraction tended to lie below 4%. However, false positives frequently occurred within the lower total creatine kinase activity range.

Creatine Kinase↗

PubMed2003

Presence of (phospho)creatine in developing and adult skeletal muscle of mice without mitochondrial and cytosolic muscle creatine kinase isoforms.

We assessed the relationship between phosphocreatine (PCr) and creatine (Cr) content and creatine kinase (CK) activity in skeletal muscle of mice. The PCr and total Cr (tCr) concentrations, as well as CK activity, in hindlimb muscles of mice, with or without the cytosolic and mitochondrial isoforms of muscle creatine kinase (wild-type or CK--/-- mice), were determined by in vivo magnetic resonance (MR) spectroscopy and by biochemical means during postnatal growth and adulthood. In wild-type muscle the [tCr], PCr/ATP ratio and CK activity increased rapidly in the first 4-7 weeks. Remarkably, CK--/-- mice showed a similar increase in the PCr/ATP ratio during the first month in the presence of only minor brain-type BB-CK activity. Uptake of Cr in muscle was seemingly unrelated to CK activity as tCr increased in the same way in the muscles of both mouse types. At older ages the PCr/ATP ratio decreased in CK--/-- muscles, in contrast to wild-type where it still slowly increased, whereas [tCr] was similar for muscle of both mouse types. Using a new in vivo MR approach with application of [4-13C]Cr, a lower PCr/tCr ratio was also observed in CK--/-- muscle. From these data it follows that in vivo global ATP levels at rest are similar in the presence or absence of CK. Although Cr could still be converted to PCr in mature CK--/-- muscle, the immediate availability of PCr decreased, and PCr became partly inconvertible at older ages. Apparently, catalysis of the CK reaction by BB-CK, although significant in muscles of newborn mice, gradually declines to very low levels in adulthood. Part or all of this BB-CK may arise from satellite cells fusing with myotubes, a process that is most active during the first months of life. Finally, our observation that the MR and chemical assessment of muscle [tCr] and PCr/tCr ratio were similar for all mice does not support the existence of a significant MR-invisible or immobile pool of Cr, with a role for CK in this phenomenon.

Adenylate Kinase↗

PubMed2006

Creatine and antioxidant treatment prevent the inhibition of creatine kinase activity and the morphological alterations of C6 glioma cells induced by the branched-chain alpha-keto acids accumulating in maple syrup urine disease.

Accumulation of the branched-chain alpha-keto acids (BCKA), alpha-ketoisocaproic acid (KIC), alpha-keto-beta-methylvaleric acid (KMV), and alpha-ketoisovaleric acid (KIV) and their respective branched-chain alpha-amino acids (BCAA) in tissues and biological fluids is the biochemical hallmark of patients affected by the neurometabolic disorder known as maple syrup urine disease (MSUD). Considering that brain energy metabolism is possibly altered in MSUD, the objective of this study was to determine creatine kinase (CK) activity, a key enzyme of energy homeostasis, in C6 glioma cells exposed to BCKA. The cells were incubated with 1, 5, or 10 mM BCKA for 3 h and the CK activity measured afterwards. The results indicated that the BCKA significantly inhibited CK activity at all tested concentrations. Furthermore, the inhibition caused by the BCKA on CK activity was totally prevented by preincubation with the energetic substrate creatine and by coincubation with the N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, indicating that deficit of energy and nitric oxide (NO) are involved in these effects. In contrast, other antioxidants such as glutathione (GSH) and trolox (soluble Vitamin E) were not able to prevent CK inhibition. In addition, we observed that the C6 cells changed their usual rounded morphology when exposed for 3 h to 10 mM BCKA and that creatine and L-NAME prevented these morphological alterations. Considering the importance of CK for brain metabolism homeostasis, it is conceivable that inhibition of this enzyme by increased levels of BCKA may contribute to the neurodegeneration of MSUD patients.

Animals↗

PubMed1996

Differential effects of creatine depletion on the regulation of enzyme activities and on creatine-stimulated mitochondrial respiration in skeletal muscle, heart, and brain.

Guanidinopropionic acid (GPA), an analogue of creatine (Cr), is known to inhibit Cr uptake by cells. The metabolic effects of chronic Cr depletion on brain, heart and soleus muscle of rats were studied. In GPA hearts and soleus muscle, total specific creatine kinase (CK) activity was decreased by approx. 40% compared to controls, whereas in brain this same activity was elevated by a factor of two. Immunoblot analysis of soleus mitochondria from GPA rats showed an approximate 4-fold increase in Mi-CK protein and a concomitant 3-fold increase in adenine nucleotide translocator (ANT) protein, when compared to control. In GPA-fed rats, the specific activities of adenylate kinase (ADK) and succinate dehydrogenase were significantly higher in brain and soleus (2-fold), but heart remained the same. However, hexokinase (HK) decreased by approx. 50% both in heart and soleus, indicating that muscle and brain follow different strategies to compensate the energy deficit caused by creatine depletion. Skinned muscle fibres from Cr-depleted soleus attained approx. only 70% maximum state 3 respiration with 0.1 M ADP in the presence of 10 mM Cr compared to 100% in control fibres. This defect in Cr stimulated respiration was also seen in isolated heart mitochondria, but was normal in those from brain. The observed deficit of Cr-stimulated respiration, the significant accumulation of Mib-CK and ANT, concomitant with the formation of Mib-CK rich intra-mitochondrial inclusions shown by electron microscopy, indicate that Mib-CK function and coupling to oxidative phosphorylation (OXPHOS), is impaired in these abnormal mitochondria. In addition, our results show tissue-specific metabolic compensations to Cr depletion.

Adaptation, Physiological↗

PubMed2002

Myoglobin, creatine kinase MB isoforms and creatine kinase MB mass in early diagnosis of myocardial infarction in patients with acute chest pain.

OBJECTIVES: Measurements of myoglobin and creatine kinase (CK)-MB isoforms have been suggested to be sensitive tests for the early diagnosis of myocardial infarction (MI). We have investigated the utility of myoglobin, creatine kinase (CK)-MB isoforms and creatine kinase MB mass (CK-MBm) in early diagnosis of MI using cardiac troponin T (cTnT) positivity as a reference. DESIGN AND METHODS: The study population comprised 440 patients who had had chest pain for less than 12 h. Patients were divided into cTnT negative (cTnT-) or cTnT positive (cTnT+) patients (concentration of cTnT >0.1 microg/L at two different time points during 72 h). RESULTS: At the time of admission to the emergency department receiver operating characteristics (ROC) curves of CK-MB isoforms and CK-MBm were not better than that of myoglobin. Six hours after admission CK-MB isoforms and CK-MBm provided statistically significantly larger areas under the curve (AUC) than myoglobin (p < 0.01). When ROC curves were related to the onset of chest pain (< 3 h, 3-6 h, and > 6 h) there were no significant differences between the cardiac markers studied. CONCLUSIONS: According to the present findings, CK-MB isoforms or myoglobin offer no advantage over CK-MBm as early markers of myocardial infarction.

Aged↗

PubMed1998

Maintained coupling of oxidative phosphorylation to creatine kinase activity in sarcomeric mitochondrial creatine kinase-deficient mice.

The importance of mitochondrial creatine kinase (mi-CK) in oxidative muscle was tested by studying the functional properties of in situ mitochondria in saponin-skinned muscle fibres from sarcomeric mi-CK-deficient (mutant) mice. Biochemical analyses showed that the lack of mi-CK in mutant muscle was associated with a decrease in specific activity of MM-CK in mutant ventricle, and increase in mutant soleus (oxidative) muscle. Lactate dehydrogenase activity and isoenzyme analysis showed an increased glycolytic metabolism in mutant soleus. No change was observed in ventricular muscle. In control animals, the apparent K(m) of mitochondrial respiration for ADP in ventricle and soleus (232 +/- 36 and 381 +/- 63 microM, respectively) was significantly reduced in the presence of creatine (52 +/- 8 and 45 +/- 12 microM, respectively). There was no change in the K(m) in oxidative fibres from mutant mice (258 +/- 27 and 399 +/- 66 microM, respectively) compared with control, though surprisingly, it was also significantly decreased in the presence of creatine (144 +/- 8 and 150 +/- 27 microM, respectively) despite the absence of mi-CK. It is proposed that in mutant (and perhaps normal) oxidative tissue, cytosolic MM-CK can relocate to the outer mitochondrial membrane, where it is coupled to oxidative phosphorylation by close proximity to porin, and the adenine nucleotide translocase. Such an effect can preserve the functioning of the CK shuttle and the energetic properties of mi-CK deficient tissue.

Animals↗

PubMed1986

Beta-blockers, plasma total creatine kinase and creatine kinase myocardial isoenzyme, and the prognosis of subarachnoid hemorrhage.

Under double-blind randomized conditions the effects of early intervention with oral propranolol or a placebo were studied in 51 cases of subarachnoid hemorrhage. Eleven out of 23 patients randomly assigned to placebo had a poor outcome at 6 months, while 2 of the 28 patients randomly assigned to propranolol had a poor outcome (p less than 0.001). Patients with a poor outcome on the placebo had significantly higher mean plasma total creatine kinase levels (742 IU, standard error of the mean +/- 233 IU) on the fifth day after subarachnoid hemorrhage than patients with a good outcome on the placebo (108 +/- 20 IU; p less than 0.05). A raised plasma creatine kinase myocardial isoenzyme was associated with a particularly poor outlook in patients receiving the placebo, in contrast to those taking a beta-blocker. Clinical outcome and plasma creatine kinase levels in patients taking atenolol (hydrophilic) were similar to those observed in patients receiving propranolol.

Adrenergic beta-Antagonists↗

PubMed1991

Simultaneous occurrence of the MB isoenzyme of creatine kinase and macro creatine kinase type 1 in a patient with acute myocardial infarction.

When the immunoinhibition method is used for differentiation of isoenzymes of creatine kinase, the simultaneous occurrence of the MB isoenzyme and variants of macro creatine kinase may lead to misinterpretation in the diagnosis of acute myocardial infarction. We describe the case of an elderly woman in whom the MB isoenzyme and the type 1 variant of macro creatine kinase were found simultaneously in her serum after acute myocardial infarction. It proved possible to identify the MB isoenzyme rapidly using a fast enzymeimmunoassay.

Aged↗

PubMed1996

Creatine kinase: the characteristics of the enzyme regenerated from the thio-methylated creatine kinase reflect a differentiation in function between the two reactive thiols.

The activity of S-thiomethyl-modified creatine kinase is due to regeneration of the free thiol (Hou and Vollmer, Biochim Biophys Acta (1994) 1205, 83-88). Characteristics of enzyme regenerated from the S-thiomethyl-modified creatine kinase are reported in the present study. The intrinsic fluorescence of the regenerated enzyme is similar to that of the native enzyme in the presence or absence of the dead-end complex. Regenerated CK (rCK) with full activity has only one reactive thiol. The rate constant of the rCK-reactive thiol reacting with DTNB is close to that of the slow phase of the reactive thiols of the native enzyme. If the IAM-modified rCK is treated with the same method as that for obtaining the rCK, the thiol-methylated reactive thiol of the rCK is reduced to a free SH and a regenerated enzyme, RCK, is produced with about 10% of the rCK activity. Therefore, the different roles of the two reactive thiols of creatine kinase may stem from the characteristics of the rCK, which suggests that only one of the two reactive thiols is related to the activity of the enzyme and the slower phase thiol (the first SH) in the modification reaction with DTNB is directly related to the enzymatic activity, while the faster phase thiol (the second SH) assists the first SH. This compensatory mechanism is proposed in the present study to interpret the dispute on the reactive SH role in the enzymatic catalysis.

Animals↗