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)

Plasma zinc, iron, copper, and selenium and selected blood proteins were measured in 66 men before (BHW) and after (AHW) a 5-d period of sustained physical and psychological stress called Hell Week. Recovery blood samples were obtained from 26 men 7 d after Hell Week. Dietary intakes were determined BHW and during Hell Week; zinc, iron, copper, and selenium intakes during Hell Week averaged 23.6 +/- 3.4 mg/d, 35.4 +/- 3.9 mg/d, 3.0 +/- 0.5 mg/d, and 92.5 +/- 26.7 micrograms/d, respectively. C-reactive protein was detected in only five subjects BHW and in all subjects AHW. Zinc, iron, selenium, and albumin decreased by 33%, 44%, 12%, and 9%, respectively, whereas ferritin, ceruloplasmin, and creatine kinase concentrations increased AHW by 59%, 8%, and 266%, respectively. Haptoglobin concentrations increased 57% in 30 subjects but decreased 32% in 23 subjects AHW. The biochemical changes were transitory because protein (except ferritin) and mineral concentrations were similar to BHW values 7 d after Hell Week. Hell Week induced changes characteristic of an acute-phase response in physically active men.
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PMID:Biochemical indices of selected trace minerals in men: effect of stress. 198 37

There are about one billion patients with iron deficiency anaemia all over the world. Recently, researchers have reported successively that stress can cause decrease of serum iron, in consistent with our studies showing that heat exposure and acceleration stress led to significant decrease of serum iron in rats. However, so far whether pure psychological stress can cause decrease of serum iron and consequently affect erythropoiesis has not been reported. To study the characteristic effects of psychological stress on serum iron and erythropoiesis, and to establish an useful experimental basis for further study involving how sufficient intake of dietary iron causes decrease of serum iron and the consequent effects on physiological function of the human body. Psychological stress was administered to 20 rats with Communication Box system. On the 7th and 14th day after administration, 10 rats were executed, respectively, and the rat blood and femoral bone marrow were collected for analysis of serum iron (SI), serum ferritin (SF), serum transferrin receptor (sTfR), haemoglobin (Hb), red blood cell count (RBC), RBC distribution width (RDW), mean corpuscular volume (MCV), serum erythropoietin (EPO) and bone marrow iron. Experimental data were statistically analysed with SPSS 11.0. For rats analysed on the 7th and 14th day in psychological stress group, (1) femoral bone marrow iron was significantly decreased; (2) serum iron was decreased by 28.6% (P < 0.01) and 27.5% (P < 0.01); (3) Hb was decreased by 10.0% (P < 0.01) and 12.8% (P < 0.01), RBC count was decreased by 5.1% (P < 0.05) and 9.8% (P < 0.01), MCV was decreased by 1.7% (P < 0.05) and 7.3% (P < 0.01), RDW was increased by 10.7 and 22.5%; (4) serum ferritin, transferrin receptor and EPO showed no significant changes in comparison with controls after 7-day administration, but serum ferritin and EPO were decreased by 23.8 and 12.3% while transferrin receptor increased by 31.5% after 14-day administration. For rats receiving different period of pure psychological stress: (1) serum iron and bone marrow iron showed significant decrease compared with the controls; (2) erythropoiesis was significantly inhibited; however, (3) how psychological stress affects serum iron and erythropoiesis need to be further investigated.
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PMID:Effects of psychological stress on serum iron and erythropoiesis. 1854 64

Oxidative damage induced by abnormal iron accumulation in the brain is a primary cause of many neurodegenerative diseases, while the reason for iron deposition remains unclear. A previous study reported that various kinds of stress could cause a change in iron level and psychological stress (PS) was a risk factor for neuron death. In the present study we investigated the influence of PS on iron metabolism in rat brain. The results showed that both total iron and non-protein-bound-iron (NPBI) levels were higher in the cerebral cortex, hippocampus and striatum of PS rats. The levels of iron regulatory factors, including transferrin receptor 1 (TfR1), ferritin (Fn), and iron regulatory protein1 (IRP1), were all changed in the iron deposition regions of the PS-exposed rat brain, accompanied by intensified oxidative stress. It is concluded that PS can increase the intake of iron in some regions of brain and subsequently causes regional iron accumulation, indicating PS might be an important reason for iron deposition-caused neurodegenerative diseases.
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PMID:Psychological stress induces dysregulation of iron metabolism in rat brain. 1855 17

We have previously demonstrated that psychological stress (PS) can cause iron to accumulate in the cerebral cortex, hippocampus, and striatum of rats. However, why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated. In the present study, we investigated the influence of PS on the low molecular weight iron pool (LMWIP) in the rat brain. The results showed that: (1) PS significantly expanded LMWIP in the cerebral cortex, hippocampus, and striatum in rats; (2) PS caused derangement of pyramidal cells and reduced the layers of pyramidal CA1 and CA2 neurons; (3) PS exposure greatly lowered the expression of ferritin (Fn) and hephaestin (HP) in the rat cortex and hippocampus; and (4) PS decreased superoxide dismutase, glutathione peroxidase, and glutathione level and increased malondialdehyde level in the cerebral cortex, hippocampus, and striatum in rats. These results indicated that PS could expand LMWIP significantly, which may be attributed to PS-induced decrease in Fn, HP expression, and the subsequent reduction in iron storage and utilization, and expansion of LMWIP could in turn lead to aggravation of oxidative damage.
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PMID:Psychological stress expands low molecular weight iron pool in cerebral cortex, hippocampus, and striatum of rats. 2199 66

Physiological responses to psychological stressors are protective in acute fight or flight situations; however, there is increasing evidence suggesting the detrimental impact of chronic psychological stress on disease. Chronic stress has been associated with inflammation, poor prognosis, increased morbidity, and poor outcome in many diseases including atherosclerosis, cancer, and pulmonary disease. Given the systemic impact of stress, and the role of the hematopoietic system as a rapid responder to homeostatic insults, we hypothesized that early blood profile changes and biochemical alterations could be detected in a model of chronic stress. To test this hypothesis, a variation of the chronic unpredictable stress (CUS) model was employed. Following 10 days of CUS, C57BL/6 mice exhibited a chronic-stress-associated corticosterone profile. Complete blood count (CBC) revealed mild normochromic, normocytic anemia, and reduced monocyte and lymphocyte count. Serum analysis demonstrated hypoferremia with unchanged total iron binding capacity and serum ferritin levels. These findings are consistent with clinical diagnostic parameters for anemia of chronic disease and indicate that CUS results in significant changes in blood and serum biochemical profile in C57BL/6 mice. These studies identify early changes in blood parameters in response to CUS and identify hematopoietic and biochemical alterations that are often associated with increased morbidity in patients experiencing chronic-stress-associated mental health disease.
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PMID:Early Blood Profile of C57BL/6 Mice Exposed to Chronic Unpredictable Stress. 3106 43