Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anthracycline antibiotics, including adriamycin (ADM), are widely used to treat various human cancers, but their clinical use has been limited because of their cardiotoxicity. ADM is especially toxic to heart tissue. The mechanisms responsible for the cardiotoxic effect of ADM have been very/extremely controversial. This review focuses on the participation of free radicals generated by ADM in the cardiotoxic effect. ADM is reduced to a semiquinone radical species by microsomal NADPH-P450 reductase and mitochondrial NADH dehydrogenase. In the presence of oxygen, the reductive semiquinone radical species produces superoxide and hydroxyl radicals. Generally, lipid peroxidation proceeds by mediating the redox of iron. ADM extracts iron from ferritin to form ADM-Fe3+, which causes lipid peroxidation of membranes. These events may lead to disturbance of the membrane structure and dysfunction of mitochondria. However, superoxide dismutase and hydroxyl radical scavengers have little effect on lipid peroxidation induced by ADM-Fe3+. Alternatively, ADM is oxidatively activated by peroxidases to convert to an oxidative semiquinone radical, which participates in inactivation of mitochondrial enzymes or including succinate dehydrogenase and creatine kinase. Here, we discuss the activation of ADM and the role of reductive and oxidative ADM semiquinone radicals in the cardiotoxic effect of this antibiotic.
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PMID:[Free radicals mediate cardiac toxicity induced by adriamycin]. 1457 31

The aim of the study was to assess the within-subject (day-to-day) variability for iron status variables: ferritin (ferr) and soluble transferrin receptor (sTfR) concentrations in plasma and the sTfR/log ferr index in athletes subjected daily to high physical loads. Blood was sampled in the morning from 8 healthy male elite judoists, aged 20 - 31 years, for 10 consecutive days while at training camp. Mean concentrations of ferritin and sTfR in plasma for the 10 day period were 32.0. 1.771(+/-1) and 2.41. 1.324(+/-1) mg/l, respectively. The average within-subject, day-to-day variability for ferritin was 27.4 % (range: 16 - 44 %), and was much lower for sTfR (6.7 %; range: 4 - 15 %). Ferritin concentrations were significantly, albeit weakly, correlated with training loads on the preceding day (r = 0.256; p < 0.05) and with creatine kinase (CK) activities on the same day (r = 0.397; p < 0.001), while sTfR did not correlate with either training loads or CK activities. Mean day-to-day variability for the sTfR/log ferr index was 11.8 % (range: 5 - 21 %), i.e. markedly lower than for ferritin. Although the physical load-induced changes in iron metabolism indices in male subjects were similarly oriented as in the earlier reported female ones representing the same sport, the magnitude of those changes was less pronounced than in the females. This was evidenced by a markedly lower within-subject day-to-day variability in ferritin, still significant but weak correlation between load magnitude and ferritin levels, and a significant, negative correlation between ferritin and sTfR concentrations, not found previously in the female athletes. However, despite lower variability in ferritin than in women, the exercise-induced ferritin increases in male athletes might make a reliable assessment of iron stores in them difficult. The present results confirm our earlier reports that sTfR levels are stable under high physical loads, thus making them a useful indicator of iron status. Also sTfR/log ferr index is of a much higher diagnostic value than ferritin, despite high variability of the latter. That index is particularly valuable in detecting iron-deficient erythropoiesis.
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PMID:The effects of physical exercise on the concentrations of ferritin and transferrin receptor in plasma of male judoists. 1545 32

A 52 year-old woman noticed general fatigue, polyarthralgia, and muscle weakness of lower extremities in October 2001. In December, she felt difficulty in walking due to muscle weakness. In January 2002, she admitted another hospital because of dyspnea on exertion and edema of lower extremities. Laboratory test revealed leukocytopenia, the elevation of creatine kinase and positive anti-U1-RNP antibodies. Her chest computed tomography (CT) showed severe interstitial pneumonia. Cardiac echogram revealed that she had pericardial effusion and pulmonary hypertension. Then she was transferred to Keio University Hospital and she was diagnosed as having mixed connective tissue disease (MCTD) manifestating myositis, interstitial pneumonia, pulmonary hypertension and pericarditis. Prednisolone (PSL) 60mg daily following to methylprednisolone (mPSL) pulse therapy was begun and her symptoms were gradually improved. In middle of February, she complained of high fever over 39.0 degrees C. Bacterial culture tests were negative and laboratory data indicated pancytopenia and a high level of serum ferritin. Bone marrow aspiration revealed hemophagocytosis in bone marrow specimens and she was diagnosed as having hemophagocytic syndrome associated with MCTD. mPSL pulse therapy was not effective and intermittent cyclophosphamide pulse therapy (IV-CY) was performed resulting in improvement of the symptoms. This case suggested the effectiveness of IV-CY therapy in patients with corticosteroid-resistant HPS associated with connective tissue diseases.
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PMID:[A case of mixed connective tissue disease successfully treated for hemophagocytic syndrome with intermittent intravenous injection of cyclophosphamide]. 1555 24

Elevated cardiac troponin T (cTnT) has been associated with shorter survival in hemodialysis patients. Moreover, intravenous (IV) iron treatment has been held responsible for oxidative stress and accelerated atherosclerosis in these patients. In the present study, we investigated the relationship between cTnT concentration, IV iron treatment, and parameters of iron status. In addition, parameters of oxidative stress, inflammation, and atherosclerosis were evaluated. Predialysis blood samples of 78 chronic hemodialysis patients were analyzed for cTnT, malondialdehyde, creatine kinase (CK), and CK-isoenzyme MB (CK-MB). In addition, the mean value of predialysis serum samples collected during the last year, were considered for homocysteine, ferritin, iron, iron binding capacity, blood cell counts, blood urea nitrogen, creatinine, albumin, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), calcium, phosphate, iPTH, cholesterol, and triglyceride. The quantity of IV iron sucrose administered during the last two years was counted from the patients' files. Echocardiography, all events related to ischemic heart disease, and urine volume were also recorded. Elevated cTnT levels (> or =0.10 ng/mL) were found in 18 patients (23.1%). The amount of iron administered was 2264+/-1871 mg with a range 0-7000 mg. Patients with elevated cTnT levels received more IV iron than those with normal cTnT (3692+/-1771 vs. 1761+/-1595 mg, p<0.001). The serum ferritin level was higher in patients with elevated cTnT (median levels; 477 vs. 288 ng/mL; P<0.05). Patients with elevated cTnT were longer on dialysis compared to those with normal levels (median times; 35.5 vs. 15 months, P<0.01) and regression analysis identified the amount of administered iron as an independent factor for elevated cTnT (P<0.01). Intravenous iron treatment and high ferritin concentration are related to high cTnT level, which has previously been incriminated as a survival marker in hemodialysis patients.
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PMID:Elevated cardiac troponin T in hemodialysis patients receiving more intravenous iron sucrose. 1560 Feb 58

Chronic graft-vs.-host disease (cGVHD) occurs in 20-50% of patients who survive for at least 100 d after allogeneic stem cell transplantation (SCT). cGVHD includes scleroderma-like skin changes, chronic cholangitis, obstructive lung disease and general wasting syndrome. Polymyositis or myopathy are rare manifestations of cGVHD with approximately 40 reported cases. Polymyositis accompanied by hemosiderin deposits in cGVHD has been reported only once, and there are no reports on lipofuscin deposits in skeletal muscle cells in cGVHD. We report here on a 56-yr-old male who underwent allogeneic SCT in 1999 for osteomyelofibrosis and progressive hematopoietic insufficiency. In February 2004, the patient was hospitalized for progressive muscular weakness with loss of the ability to walk. Laboratory tests demonstrated normal values for serum creatine kinase, aldolase and lactic dehydrogenase; the ferritin level was highly elevated. The femoral muscle biopsy showed mostly perifascicular atrophy as well as numerous subsarcolemmal hemosiderin and lipofuscin deposits. Intravenous administration of the chelating agent deferoxamine was ineffective. Three weeks later the patient died of aspiration pneumonia. Interestingly, autopsy disclosed moderate hemosiderin deposits in the liver, the organ usually involved in hemosiderosis.
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PMID:Hemosiderin deposits in chronic graft-vs.-host disease related myopathy. 1631 67

In the present study we used patient data to calculate laboratory-specific indirect reference intervals. These values were compared with reference intervals obtained for a healthy group according to recommendations of the International Federation of Clinical Chemistry and Laboratory Medicine and manufacturer suggestions. Laboratory results (422,919 records) from all subjects of 18-45 years of age over a 1-year period were retrieved from our laboratory information system and indirect reference intervals for 40 common analytes were estimated using a modified Bhattacharya procedure. Indirect reference intervals for most of the biochemical analytes were comparable, with small differences in lower [alkaline phosphatase (ALP) (male), alanine aminotransferase (ALT), creatine kinase, iron (male), total iron-binding capacity, folic acid, calcium (female), lactate dehydrogenase (LDH), lipoprotein (a) [Lp(a)], thyroid-stimulating hormone (TSH), total triiodothyronine (T(3)), direct bilirubin, apolipoprotein A-I (apoA-I), glucose, homocysteine, total cholesterol, ferritin, total protein, ceruloplasmin, sodium, blood urea nitrogen (BUN) and uric acid (female)] and/or upper limits [albumin, ALP (male), amylase, apoA-I, creatine kinase-MB (CK-MB), total iron-binding capacity, phosphorus, glucose, total cholesterol, gamma-glutamyltransferase (gamma-GT), magnesium, total protein, high-density lipoprotein cholesterol (HDL-C), total T(3), ALP (male), ALT, aspartate aminotransferase (AST) (male), direct bilirubin (male), creatine kinase, iron, folic acid (female), Lp(a), uric acid and triglycerides], to the reference intervals determined for healthy subjects in our laboratory. The indirect reference intervals, with the exception of a few parameters (creatinine, direct total bilirubin, calcium, BUN and potassium), were not similar to the reference intervals suggested by the manufacturers. We conclude that laboratory-specific reference intervals can be determined from stored data with a relatively easy and inexpensive method. Indirect reference intervals derived from stored data may be particularly suitable for the evaluation of results for the presenting population.
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PMID:Use of total patient data for indirect estimation of reference intervals for 40 clinical chemical analytes in Turkey. 1677 35

The distinction between positive and negative training adaptation is an important prerequisite in the identification of any marker for monitoring training in athletes. To investigate the glutamine responses to progressive endurance training, twenty healthy males were randomly assigned to a training group or a non-exercising control group. The training group performed a progressive (3 to 6 x 90 minute sessions per week at 70 % V.O (2max)) six-week endurance training programme on a cycle ergometer, while the control group did not participate in any exercise during this period. Performance assessments (V.O (2max) and time to exhaustion) and resting blood samples (for haemoglobin concentration, haematocrit, cortisol, ferritin, creatine kinase, glutamine, uric acid and urea analysis) were obtained prior to the commencement of training (Pre) and at the end of week 2, week 4 and week 6. The training group showed significant improvements in time to exhaustion (p < 0.01), and V.O (2max) (p < 0.05) at all time points (except week 2 for V.O (2max)), while the control group performance measures did not change. In the training group, haemoglobin concentration and haematocrit were significantly lower (p < 0.01) than pretraining values at week 2 and 4, as percentage changes in plasma volume indicated a significant (p < 0.01) haemodilution (+ 6 - 9 %) was present at week 2, 4 and 6. No changes were seen in the control group. In the training group, plasma glutamine (week 2, 4 and 6), creatine kinase (week 2 and 4), uric acid (week 2 and 4) and urea (week 2 and 4) all increased significantly from pretraining levels. No changes in cortisol or ferritin were found in the training group and no changes in any blood variables were present in the control group. Plasma glutamine was the only blood variable to remain significantly above pretraining (966 +/- 32 micromol . 1 (-1)) levels at week 6 (1176 +/- 24 micromol . 1 (-1); p < 0.05) The elevation seen here in glutamine levels, after 6 weeks of progressive endurance training, is in contrast to previous reports of decreased glutamine concentrations in overtrained athletes. In conclusion, 6 weeks of progressive endurance training steadily increased plasma glutamine levels, which may prove useful in the monitoring of training responses.
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PMID:Monitoring 6 weeks of progressive endurance training with plasma glutamine. 1702 35

This review accounts for the current development in microfluidic immunosensing chips. The basic knowledge of immunoassay in relation to its microfluidic material substrate, fluid handling and detection mode are briefly discussed. Here, we mainly focused on the surface modification, antibody immobilization, detection, signal enhancement and multiple analyte sensing. Some of the clinically important currently implemented on the microfluidic immunoassay chips are C-reactive protein (CRP), prostate specific antigen (PSA), ferritin, vascular endothelial growth factor (VEGF), myoglobin (Myo), cardiac troponin T (cTnT), cardiac troponin I (cTnI), and creatine kinase-cardiac muscle isoform (CK-MB). The emerging microfludic immunosensor technology may be a promising prospect that can propel the improvement of clinical and medical diagnosis.
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PMID:Current development in microfluidic immunosensing chip. 1829 63

The goal of this study was the evaluation of specific markers of myocardial injury that includes CK-MB and troponin I in major thalassemic patients. Regular blood transfusion is the main treatment in major thalassemia. One of the most important complications of regular blood transfusion is iron overload that eventually involves many organs like heart and cause myocardial injury. Sixty patients with transfusion-dependent major thalassemia, at the age range of 8 to 15 years in Tabriz Pediatric Medical Center were chosen. Measurement of Hb, Hct and serum ferritin were performed in hospital laboratory, but total serum Creatine Kinase (CK) by photometric and isoenzyme of CK-MB by immunologic DGKC and cardiac troponin I (cTnI) were tested by ELISA methods in Shaheed Madani heart center laboratory before blood transfusion. For all patients echocardiography and ECG assessment of cardiac function were done by a pediatric cardiologist and results were statistically analyzed. Forty nine patients (group A) had normal left ventricular ejection fraction (LVEF = 50-70%) and 11 patients (group B) had reduced LVEF (20-45%). There was no statistical difference between two groups in average volume of blood transfusion (p = 0.074). Although total CK and CK-MB isoenzyme were higher in group B but there was no statistically meaningful difference between two groups (p = 0.123, p = 0.111). Troponin I also was higher in group B but statistically analysis showed no correlation between cardiac function and troponin I level in these groups (p = 0.827). This study showed that cardiac markers are not helpful for recognition of cardiac involvement in major thalassemia.
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PMID:Cardiac involvement of major thalassemia and evaluation of total serum creatine kinase and creatine kinase-mB isoenzyme and cardiac troponinI in these patients. 1881 Sep 80

Coal dust causes lung diseases in occupational exposure. Reactive oxygen species have been implicated in the pathogenesis of its toxicity. In this study, serum enzymes, lipid profile and other biochemical values with oxidant/antioxidant status in whole blood and serum of central heating system workers (CHSW; the persons responsible for heating the apartment with coal) were determined to reflect the cell injury. Blood samples were obtained from CHSW (n = 25) and healthy individuals (n = 25). All values were measured in whole blood and serum. ANOVA was used for the estimation of statistical data. In the group of CHSW, creatinine, ferritin, alanin aminotransferase, aspartate aminotransferase, creatine phosphokinase, gamma glutamyl transferase, lactate dehydrogenase and glutathione reductase activities as well as triglyceride, very low density lipoprotein, protein carbonyl and malondialdehide were significantly higher, while transferrin, high density lipoprotein and catalase (CAT) activities were lower than the group of healthy individuals. This result is consistent with hypothesis that respirable coal dust generates lipid and protein oxidation and induces leakage of serum enzymes by cell damage. It also leads to imbalance in antioxidant defense system, lipid profile and other biochemical parameters.
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PMID:Increased occupational coal dust toxicity in blood of central heating system workers. 2072 14


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