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)

An association has been shown between iron deficiency and a low gastric acidity while the latter is known to increase susceptibility to cholera. This study was undertaken to ascertain whether iron deficiency is a risk factor for contracting cholera. The subjects were 60 adult males-30 with cholera admitted to ICDDR,B and 30 controls matched for age, sex and socio-economic status from the same household or immediate neighbourhood of the index case. Fingerstick blood was taken from all subjects to estimate the haematocrit, and serum ferritin concentration by an ELISA. The mean ferritin level of the study group was 38.7 ng/100 ml, in the controls. There was a significant difference in the serum ferritin level between the groups (P less than 0.005), Wilcoxon Sign Rank test for matched pairs suggesting that cholera patients tend to have lower serum ferritin concentration. Further prospective studies are required to define the possible association between iron deficiency and cholera more accurately.
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PMID:Serum ferritin and cholera. A prospective study. 175 Jan 1

Conflicting data have been reported on tumor marker determination in gastric juice. In the present study the effect of pH variations on both antibody-antigen binding and the immunologic stability of the antigen were evaluated for the radioimmunoassay of carcinoembryonic antigen, CA19-9, tissue polypeptide antigen, and ferritin. A significant inhibition of antibody-antigen binding was constantly found in acidic conditions. Antigen concentration was lower in acidified than in untreated samples, possibly due to the carryover of acidity in the incubation mixture. Neutralization of acidified samples partly improved recovery of carcinoembryonic antigen and CA19-9. Tissue polypeptide antigen and ferritin were not recovered by neutralization in samples with pH less than 4.5, suggesting an irreversible damage of the immunologic characteristics of the two antigens. From the present data we conclude that an accurate validation of methods and a rigorous standardization of sample collection are mandatory for tumor marker determination by radioimmunoassay in gastric juice.
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PMID:Tumor marker radioimmunoassays in gastric juice. Methodologic drawbacks due to pH variations. 316 87

Lactic acid 4 mM acted as a lipoperoxidant by increasing production of thiobarbituric acid-reactive substances (TBARS) in rat kidney slices and homogenates. This effect occurred mainly when slices and homogenates were incubated in a pH 5.4 medium conductive to full expression of compound acidity. TBARS increase was only slight when incubation was performed in Krebs buffer, pH 7.4. Moreover, sodium lactate 4 mM increased TBARS production only when homogenates were incubated in the pH 5.4 medium. Deferoxamine (1 mM) inhibited the prooxidant effect of lactic acid 4 mM, and TBARS increase was correlated with iron release. The iron mobilized may come from reserves where it is weakly bound or from ferritin; and ascorbic acid, present in low quantities in kidney, might trigger the release of this product.
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PMID:Iron- and lactic acid-induced lipid peroxidation in rat kidney homogenates and slices. 811 16

We investigated the iron release from ferritin by irradiation from a white fluorescent light in the absence or presence of ADP. Irradiation of a ferritin solution at 17,000 lx in the absence of ADP slightly induces iron release from ferritin but only at acidic pH conditions (pH 5.0 or pH 6.0). Irradiation in the presence of ADP markedly enhances iron release from ferritin under the same conditions. In the absence of irradiation, the iron release from ferritin was low even in the presence of ADP. The induction of the iron release by irradiation in the presence of ADP was also affected by various factors such as irradiation dose and acidity, but not temperature (4-47 degrees C), oxygen concentration, or free radical generations during the irradiation. The iron release during the irradiation ceased to increase by turning off the light and was found to increase again after additional irradiation. These results suggest that visible light directly induces iron release from ferritin via the photoreduction of iron stored inside ferritin.
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PMID:Iron release analyses from ferritin by visible light irradiation. 1603 68

We studied the synergistic effect of visible light and ferritin on the lipid peroxidation on a fraction of porcine photoreceptor outer segment (POS). Reaction mixtures containing the POS fraction and horse spleen ferritin were irradiated under white fluorescent light mainly at 17,000 lx or incubated under dark conditions at 37 degrees C. The lipid peroxidation was evaluated by both the thiobarbituric acid method and the ferrous oxidation/xylenol orange method. The irradiation-induced lipid peroxidation was affected by some experimental factors such as the irradiation dose and acidity of the material. When the irradiation was stopped, the lipid peroxidation was also stopped; thereafter, the re-irradiation induced lipid peroxidation. Moreover, this lipid peroxidation was inhibited by desferrioxamine, an iron chelator, or by dimethylthiourea, a hydroxyl radical scavenger, suggesting that the lipid peroxidation involves hydroxyl radicals generated via the Fenton reaction by iron ion released from ferritin. The lipid peroxidation did not take place under dark conditions or in the absence of ferritin. This study suggested the possibility that the visible light-induced lipid peroxidation of the POS fraction in the presence of ferritin may participate in the etiology of human retinal degenerative diseases as the human retina is exposed to light for life.
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PMID:In the presence of ferritin, visible light induces lipid peroxidation of the porcine photoreceptor outer segment. 1701 58

Iron deficiency, a condition currently affecting approximately 3 billion people, persists in the 21st century despite half a millennium of medical treatment. Soybean ferritin (SBFn), a large, stable protein nanocage around a mineral with hundreds of iron and oxygen atoms, is a source of nutritional iron with an unknown mechanism for intestinal absorption. Iron absorption from SBFn is insensitive to phytate, suggesting an absorption mechanism different from for the ferrous transport. Here, we investigated the mechanism of iron absorption from mineralized SBFn using Caco-2 cells (polarized in bicameral inserts) as an intestinal cell mode and analyzed binding, internalization and degradation with labeled SBFn ((131)I or fluorescent labels), confocal microscopy, and immunoanalyses to show: 1) saturable binding to the apical cell surface; dissociation constant of 7.75 +/- 0.88 nmol/L; 2) internalization of SBFn that was dependent on temperature, concentration, and time; 3) entrance of SBFn iron into the labile iron pool (calcein quenching); 4) degradation of the SBFn protein cage; and 5) assembly peptide 2 (AP2)-/clathrin-dependent endocytosis (sensitivity of SBFn uptake to hyperosmolarity, acidity, and RNA interference to the mu(2) subunit of AP2), and resistance to filipin, a caveolar endocytosis inhibitor. The results support a model of SBFn endocytosis through the apical cell membrane, followed by protein cage degradation, mineral reduction/dissolution, and iron entry to the cytosolic iron pool. The large number of iron atoms in SBFn makes iron transport across the cell membrane a much more efficient event for SBFn than for single iron atoms as heme or ferrous ions.
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PMID:Caco-2 intestinal epithelial cells absorb soybean ferritin by mu2 (AP2)-dependent endocytosis. 1835 17

The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-alpha (TNF alpha) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group 1 was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNF alpha, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNF alpha levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNF alpha levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNF alpha levels. Thus, elevated serum TNF alpha in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.
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PMID:Role of Helicobacter pylori in refractory iron deficiency anaemia. 1983 23

Osteoarthritis (OA) microenvironment is marked by matrix metalloproteinases-13 (MMP-13) overexpression and weak acidity, making it possible to develop dual-stimuli responsive theranostic nanoprobes for OA diagnosis and therapy. However, current MMP/pH-responsive systems are not suitable for OA because of their poor biocompatibility, poor degradation and non-cartilage-targeting of the responsive probes. Here we designed a novel biocompatible cartilage-targeting and MMP-13/pH-responsive ferritin nanocages (CMFn) loaded with an anti-inflammatory drug (Hydroxychloroquine, HCQ), termed CMFn@HCQ, for OA imaging and therapy. We found that CMFn could be smartly "turned on" to emit light for OA imaging in response to the level of overexpressed MMP-13 in OA microenvironment, corresponding to the degree of OA severity. Thus the light intensity detected reflected the degree of OA severity, enabling the precise disease classification by our CMFn. CMFn could be "turned off" to stop emitting light in the normal joint. CMFn@HCQ nanocages could target the cartilage and release HCQ in the OA joint specifically under acidic pH conditions in a sustained manner, prolonging the drug retention time to 14 days to remarkably reduce synovial inflammation in the OA joints. The CMFn@HCQ nanocages represent a smart dual-stimuli responsive and cartilage-targeting nanoprobes, and hold promise for imaging-guided precision therapy for OA.
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PMID:Cartilage-targeting and dual MMP-13/pH responsive theranostic nanoprobes for osteoarthritis imaging and precision therapy. 3158 65