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PubMed1995

Expression of brain-type creatine kinase and ubiquitous mitochondrial creatine kinase in the fetal rat brain: evidence for a nuclear energy shuttle.

To test the hypothesis that embryonic brain cells utilize a creatine phosphate energy shuttle, we examined the pattern of creatine kinase (CK) isoform expression and localization in the fetal rat brain. Moderate levels of CK activity are present at embryonic day 14 (7 U/mg protein) and decrease slightly until 3 days postpartum followed by a rapid, fourfold up-regulation to adult levels by 1 month (18 U/mg protein). In parallel with changes in enzyme activity, there is a biphasic and coordinate pattern of expression of brain-type CK (BCK) and ubiquitous mitochondrial CK (uMtCK) determined by nondenaturing electrophoresis and immunoblot analysis. The localization of CK isoforms was examined by immunocytochemistry, and, during the fetal period, BCK and uMtCK immunoreactivity was detected throughout the central and peripheral nervous system, especially in neuroepithelial regions of the cerebral vesicles and spinal cord. In large cells within the olfactory neuroepithelium and ventral spinal cord, differential compartmentation of CK isoforms was evident, with BCK localized primarily in cell nuclei, whereas uMtCK immunoreactivity was present in the cell body (but not within nuclei). In olfactory bulb neuroepithelium, both isoforms were expressed in the middle zone of the germinal layer associated with DNA synthesis. In embryonic skeletal and cardiac muscle, which also express BCK, the same compartmentation of BCK was seen, with BCK localized primarily in the cell nucleus of cardiac and skeletal myoblasts. These results demonstrate a coordinate pattern of expression and compartmentation of BCK and uMtCK isoforms in the fetal brain that, in some cells, provides the anatomic basis for a nuclear energy shuttle.

Animals↗
PubMed1985

Creatine kinase and creatine kinase MB in endurance runners and in patients with myocardial infarction.

Following a 100 km race creatine kinase (CK) creatine kinase MB (CKMB) activities were serially measured in well trained athletes and compared with enzyme activities in patients with acute myocardial infarction (AMI). The half-time of disappearance of CK (CKt1/2) was 1.75 +/- 0.70 days in runners who trained within the 1st week after the race, and was 0.81 +/- 0.18 days in patients with AMI, P less than 0.005. CKt1/2 in runners was shorter (1.17 +/- 0.28 days) when no training was performed in the first postrace week. CKt1/2 was linearly correlated with age (P less than 0.01) in the runners but not in the patients. CKMBt1/2 was 1.30 and 1.11 days in two runners and 0.56 +/- 0.10 days in patients with AMI (P less than 0.05). In line with histologic and enzymatic findings in skeletal muscle of long distance runners as reported by other workers, our kinetic data provide further evidence that CK and CKMB are released from muscular compartments in runners other than those in patients with AMI.

Adult↗
PubMed1983

Elevated serum creatine kinase MB and creatine kinase BB-isoenzyme fractions after ultra-marathon running.

To determine the incidence and range of serum creatine kinase MB (CK-MB) isoenzyme activity after ultra-marathon running, a popular test kit was used to measure total serum creatine kinase (CK) and CK MB-activity in 75 athletes immediately after they had completed an 88-km running race. Total serum CK activity was markedly elevated after the race (mean value: 637 U X 1(-1) and 45 (60%) runners showed abnormal CK-MB isoenzyme activities (greater than 4% of total CK activity - range 1-19%). Electrophoresis of 31 sera with either CK-MB to total CK activity greater than 4% or with total CK activity greater than 854 U X 1(-1) showed that 31 (100%) had visible CK-MM bands, 21 (68%) had visible CK-BB bands, but only 14 (44%) had visible CK-MB bands. We conclude that prolonged exercise increases the serum activity of all three CK-isoenzymes, and that the CK-MB test kit used in this study identified a greater number of sera with elevated post-race CK-MB isoenzyme activity than did electrophoresis. This discrepancy could result either from cross-reaction of elevated CK-BB activity with the test kit, or from relative insensitivity of the electrophoresis. The tissue source and long-term significance of the elevated serum CK-MB and CK-BB isoenzyme activity induced by ultra-marathon running are uncertain. Until these issues are resolved, these biochemical findings in ultra-marathon runners must be interpreted with the appropriate caution.

Creatine Kinase↗
PubMed1991

Increases of neuron-specific enolase, S-100 protein, creatine kinase and creatine kinase BB isoenzyme in CSF following intraventricular catheter implantation.

In 15 patients without acute brain injury the concentrations of Neuron-specific Enolase (NSE), S-100 Protein (S-100), Creatine Kinase (CK), and Creatine Kinase BB isoenzyme (CK-BB) in ventricular cerebrospinal fluid (CSF) were measured immediately after lateral ventricle cannulation for diagnostic or treatment purposes. From patients who were treated with a shunt another CSF sample was obtained one week after shunt implantation by puncture of the antechamber of the valve. The CSF concentrations of NSE, S-100, CK and CK-BB after cannulation were found to be of the same order as found in patients with severe head injury, stroke or subarachnoid haemorrhage. One week after shunt implantation the concentrations of S-100, CK and CK-BB had returned to normal levels in almost all patients, while the NSE concentrations remained elevated. These findings indicate that the sampling procedure may result in contamination of CSF with NSE, S-100, CK and CK-BB and they should be taken into account in the prognostic evaluation of enzyme concentrations after brain injury.

Brain Damage, Chronic↗
PubMed1985

Kinetics of serum creatine kinase and creatine kinase-MB after intracoronary thrombolysis.

The kinetics of the activity of total creatine kinase (CK) and creatine phosphokinase isoenzyme muscle-brain were investigated in 48 patients with acute myocardial infarction after successful intracoronary thrombolysis, and compared to the enzyme activities in 17 patients in whom thrombolysis failed. CK activity peaked significantly earlier after a successful thrombolysis than after an unsuccessful attempt: in patients with successful thrombolysis, CKmax = 10.5 +/- 3.7 h and in patients with an unsuccessful attempt, CKmax = 19.3 +/- 5.9 h; p less than or equal to 0.05. The area under the activity time curve after successful thrombolysis was significantly smaller than after unsuccessful thrombolysis: in patients with successful thrombolysis, CK area = 25,255 U/l per day and in patients with an unsuccessful attempt, CK area = 32,602 U/l per day; p = 0.015. There was a negative correlation between the area under the CK serum curve after successful thrombolysis, and the change of regional wall motion at the site of the acute infarct (p less than or equal to 0.05). From the smaller area under the CK curve in patients after successful thrombolysis, and the significant negative correlation of this measurement with regional left ventricular wall motion, we conclude that myocardial salvage after intracoronary thrombolysis can be assessed by serial CK measurements.

Coronary Circulation↗
PubMed1983

Tetrathionate-blocked creatine kinase as a substrate for human plasma 'creatine kinase conversion factor'.

'Creatine kinase conversion factor' has been partially purified from whole plasma. The preparation has the ability to convert slowly migrating, native CK-MM into a faster electrophoretic form through a form of intermediate mobility. These changes are accompanied by a loss in CK activity. The rates of both electrophoretic conversion and loss of enzyme activity are reduced or prevented by the presence of 2-mercaptoethanol, EDTA, or by formation of the creatine-MgADP-nitrate dead-end complex. When the thiol group essential for enzyme activity found at the CK active site is first blocked by treatment with potassium tetrathionate, full activity may be retained under conditions that fully convert CK to the faster electrophoretic forms. The conversion factor activity was not inhibited by a pre-incubation with the protease inhibitor, PMSF and the converted form of CK showed no evidence of proteolytic cleavage. The molecular basis of the chemical alteration caused by the conversion is discussed.

Creatine Kinase↗
PubMed1987

Serum creatine kinase-BB levels and cerebral cortical creatine kinase activity in senile dementia of the Alzheimer type.

A rise in serum creatine kinase-BB (CK-BB) levels has been reported previously in cases of dementia. In the present study the levels of serum CK-BB have been measured in patients clinically assessed to have senile dementia of the Alzheimer's type (SDAT) and in cognitively intact individuals, matched for age, by a specific two-site monoclonal immunoradiometric assay. No significant difference was found between the 2 groups. Total creatine kinase activity in temporal cortex (Brodmann area 21 and 22) was also found to be similar in brains from SDAT or control cases, obtained at autopsy. These results suggest no major change in the permeability of the blood-brain barrier to this enzyme in SDAT patients.

Alzheimer Disease↗
PubMed2004

Creatine and guanidinoacetate: diagnostic markers for inborn errors in creatine biosynthesis and transport.

In this study, measurements of guanidinoacetate (GAA) and creatine (Cr) in urine, plasma, and cerebrospinal fluid (CSF) were performed using stable isotope dilution gas chromatography-mass spectrometry. Both compounds were analyzed in a single analysis. Reference values were established for GAA and Cr. These values were age dependent. No differences with gender were observed. Eight guanidinoacetate methyltransferase (GAMT) deficient patients and eight creatine transporter SLC6A8 deficient patients were investigated. In urine, plasma, and CSF of GAMT deficient patients increased levels of GAA are present. The SLC6A8 deficient patients all show increased creatine/creatinine (Cr/Crn) ratio in urine demonstrating the importance of the Cr/Crn ratio as a pathognomonic marker of the SLC6A8 deficiency.

Adolescent↗
PubMed1984

Reduction of creatine kinase and creatine kinase-MB indexes of infarct size by intravenous verapamil.

In a prospective, controlled study, 29 patients were randomly allocated to receive intravenous verapamil, 5 to 10 mg/hour, for 2 days starting at a mean of 8 hours after the onset of myocardial infarction. Twenty-five patients received no specific treatment and served as control subjects. Left ventricular (LV) filling pressure in all patients was initially less than 15 mm Hg. Age, infarct localization and hemodynamic values on admission (Swan-Ganz catheter) were comparable in both groups. Maximal creatine kinase (CK) and creatine kinase-MB (CK-MB) values were markedly lower in the verapamil group than in the control group (CK 547 vs 703 U/liter, p less than 0.05; CK-MB 51 vs 68 U/liter, p less than 0.025), as was infarct weight (48 vs 65 g-Eq, p less than 0.03; CK-MB 31 vs 49 g-Eq, p less than 0.005). Arterial blood pressure was 10% lower in the verapamil group than in the control group. Systemic vascular resistance and LV filling pressure remained unchanged. Verapamil reduced myocardial infarction size by about 30% in patients without LV failure and the arterial pressure was reduced.

Blood Pressure↗
PubMed1995

Effects of physical activity on creatine phosphokinase and the isoenzyme creatine kinase-MB.

Creatine phosphokinase (CPK) and creatine kinase-MB (CK-MB) have been used extensively as diagnostic markers for myocardial infarction and skeletal muscle injury. Many factors affect the variability of serum CPK and serum CK-MB activity, especially physical activity. We discuss the influence of physical activity on muscle and serum CPK and CK-MB. The effect of acute and chronic exercise on CPK and CK-MB activity emphasizes the need to use measurements of serum CPK and CK-MB with caution when evaluating and diagnosing acute myocardial infarctions and skeletal muscle injury.

Adult↗
PubMed1998

Effect of DC shock on serum levels of total creatine kinase, MB-creatine kinase mass and troponin T.

After successful resuscitation from cardiac arrest, it is important to identify whether the event has been triggered by a myocardial infarction, since this determines subsequent investigations and management. Previous studies have shown that biochemical indices of infarction become elevated after resuscitation in patients without myocardial infarction. This can lead to overdiagnosis of myocardial infarction in the post-arrest setting. The cause of the elevated enzyme levels is not known, but may involve electrical or mechanical injury to the heart during resuscitation. In this study we aimed to identify the effects of isolated direct current shock on serum levels of creatine kinase (CK), MB creatine kinase mass (MB-CK), and troponin T, and examined the relationships between enzyme levels and the dose of electrical energy used. Thirteen patients were studied who underwent DC cardioversion for atrial fibrillation. Serum was obtained for CK, MB-CK and troponin T estimation before and 10 min after cardioversion, at hourly intervals for 8 h, and 18 h after cardioversion. Total serum CK became significantly elevated after only 3 h and rose to a peak of 1294.4 IU l(-1) (P < 0.02) at 18 h. Post-shock CK levels were strongly correlated with total shock energy (r = 0.8, P < 0.01). Serum MB-CK was significantly elevated at 18 h among patients receiving total shock energies greater than 1000 J than in those receiving lower doses, reflecting a positive correlation (r = 0.64, P < 0.05) between shock energy and peak MB-CK level. Troponin T levels were not significantly elevated after cardioversion. In conclusion, total serum CK levels become significantly elevated early after cardioversion, suggesting rapid wash-out from injured skeletal muscle. MB-CK levels become significantly elevated in individuals receiving high energy shocks, probably due to release of small quantities of the CK-MB isoform from skeletal muscle. The negligible troponin T levels seen after high energy cardioversion indicate that significant myocardial injury does not occur. Electrical injury is not likely to account for the elevated troponin T levels seen after out-of-hospital resuscitation in patients without myocardial infarction.

Aged↗
PubMed1990

Clinical application of subforms of creatine kinase MM and macro creatine kinases.

The subforms of MM isozyme of creatine kinase (ATP:creatine N-phosphotransferase, EC 2.7.3.2, CK) in sera obtained from healthy adults and patients were determined by agarose gel isoelectric focusing (IEF). The patients were classified into six groups according to serum CK-MM activities and IEF patterns. The IEF spectra offered useful information on cell hyperplasia, augmented cell membrane permeability, cell destruction and release time of CK-MM in the circulation from the cells for diagnosis, progress observation and prognosis, especially in the cases of chronic hepatic diseases, acute myocardial infarction and muscular dystrophy. Macro CKs were also determined by IEF. Macro CKs could be completely distinguished from each other, and CK isozymes consisting of macro CK type 1 could be presumed by isoelectric points.

Chromatography, Gel↗
PubMed2003

Creatine phosphate--creatine kinase in enzymatic synthesis of glycoconjugates.

[reaction: see text] Enzymatic production of glycoconjugates is hampered by expensive phosphagens such as acetyl phosphate (AcP) and phosphoenolpyruvate (PEP). Here, we introduce creatine phosphate--creatine kinase system as a novel and practical energy source in carbohydrate synthesis. This system was successfully demonstrated in the production of bioactive oligosaccharides with different sugar nucleotide regeneration systems.

Adenosine Triphosphate↗
PubMed1989

At what level of serum total creatine kinase activity can measurement of serum creatine kinase MB isoenzyme activity be omitted in suspected myocardial infarction?

The purpose of this study was to establish a discriminatory limit for serum total creatine kinase activity (CK activity) below which CK isoenzyme fractionation is unnecessary. We looked at 2610 serum samples from 1077 consecutive patients with suspected acute myocardial infraction (AMI). The CK activity was determined according to the Scandinavian recommended method. Isoenzymes of CK were separated by agarose gel electrophoresis, followed by fluorometric scanning. When the threshold for CK activity was 150 U/l, none of the samples had a creatine kinase MB isoenzyme activity (CK-MB activity) equal to or higher than 30 U/l (the diagnostic level), which has been found to differentiate between patients with AMI and those without AMI. Only 14 patients (1.3% of all patients investigated) had CK-MB activity peaks between 10 U/l (detection limit) and 30 U/l. Of these, AMI was only diagnosed in one. We recommend that CK-MB activity should be measured only when CK activity is higher than 150 U/l. This would make about 50% of all CK-MB measurements unnecessary.

Aged↗
PubMed1986

Creatine kinase and creatine kinase B-subunit in stable and unstable angina pectoris.

Repetitive ischaemic episodes may have a cumulative effect leading to irreversible myocardial cell damage with enzyme release. Using plasma creatine kinase (CK) and creatine kinase B-subunit (CK-B) concentrations this theory has been tested in forty-eight patients admitted with acute chest pain, but without ECG signs of acute myocardial infarction (AMI). The patients were classified into four groups: Fourteen patients with non-ischaemic heart disease (non-IHD), seventeen with stable angina pectoris (SAP), ten with unstable angina pectoris (UAP), and seven patients who developed AMI during the study period. The enzyme variation in non-IHD delineates the background noise, and the increased variability in AMI indicates the full scale of the enzyme signals in cases of irreversible cell damage. Patients with SAP have the same enzyme signal as the background noise in respect of both CK and CK-B. However, in UAP the signal of CK-B equals the background noise, whereas the CK signal is separated from the latter. The reason may be that the signal to noise ratio of CK-B is poor and the analytical sensitivity low. Therefore, the behaviour of CK-B in this study does not support the above theory although our findings for CK indicate that the consequence of repeated ischaemic attacks is slight enzyme release.

Angina Pectoris↗
PubMed1983

Serum creatine kinase and creatine kinase MB isoenzyme responses of post-infarction patients after a graded exercise test.

The response of total creatine kinase (CK) and the creatine kinase isoenzyme (CK MB) was studied in 22 male post-infarction patients (three to six months after myocardial infarction) after a functional graded exercise test, before entering a rehabilitation programme. Eleven subjects (group A) completed the test without developing significant electrocardiographic abnormalities. Eleven subjects (group B) showed changes that necessitated premature termination of the test. No significant differences were observed before the functional graded exercise test between the groups in serum concentration of CK, CK MB, and the percentage of CK MB to CK (MB/ CK%). The two groups were significantly different (p less than 0.01) 24 hours after the graded exercise test in CK MB and MB/CK%, but not in CK. In group B, CK and CK MB rose significantly after the graded exercise test (p less than 0.05) as did MB/CK% (p less than 0.01). In group A only CK showed a significant rise (p less than 0.05). It is probable that increases in CK MB after exercise arise from myocardial tissue efflux, reflecting reversible ischaemia. It is concluded from this study that CK MB appears to be a specific indicator of myocardial ischaemia and could, therefore, be of significant assistance in the clinical and functional assessment of the post-infarction patient.

Clinical Enzyme Tests↗