OBJECTIVETo observe the effects of iron and phosphorus on Microcystis physiological reactions.

METHODSThe experimental conditions were chosen as the light dark cycles of 16 h 8 h, 12 h 12 h, and 8 h 16 h. The cell change of morphology and life history, cell number, cell color, and cell area of Microcystis were analyzed quantitatively. According to the resource competition and Monod equation, Microcystis kinetics of phosphorus and iron were also examined.

RESULTSThe longer light time caused more special cell division, slower growth rate, and easier change of bigger cell area. The color of alga was changed from green to brown. Ks and micromax of phosphorus absorption were 0.0352 mircomol x L(-l) and 0.493 d(-1), respectively. Those of iron absorption were 0.00323 micromol x L(-1) and 0.483 d(-1).

CONCLUSIONMicrocystis bloom is more dominant than other algae.

Iron ; physiology ; Light ; Microcystis ; metabolism ; Phosphorus ; physiology

Recently, ferroptosis, an iron-dependent novel type of cell death, has been characterized as an excessive accumulation of lipid peroxides and reactive oxygen species. Emerging studies demonstrate that ferroptosis not only plays an important role in the pathogenesis and progression of chronic diseases, but also functions differently in the different disease context. Notably, it is shown that activation of ferroptosis could potently inhibit tumor growth and increase sensitivity to chemotherapy and immunotherapy in various cancer settings. As a result, the development of more efficacious ferroptosis agonists remains the mainstay of ferroptosis-targeting strategy for cancer therapeutics. By contrast, in non-cancerous chronic diseases, including cardiovascular & cerebrovascular diseases and neurodegenerative diseases, ferroptosis functions as a risk factor to promote these diseases progression through triggering or accelerating tissue injury. As a matter of fact, blocking ferroptosis has been demonstrated to effectively prevent ischemia-reperfusion heart disease in preclinical animal models. Therefore, it is a promising field to develope potent ferroptosis inhibitors for preventing and treating cardiovascular & cerebrovascular diseases and neurodegenerative diseases. In this article, we summarize the most recent progress on ferroptosis in chronic diseases, and draw attention to the possible clinical impact of this recently emerged ferroptosis modalities.
Animals ; Chronic Disease ; Ferroptosis ; physiology ; Iron ; metabolism ; Reactive Oxygen Species

Animals ; Antimicrobial Cationic Peptides ; physiology ; Carrier Proteins ; physiology ; Cation Transport Proteins ; physiology ; Ceruloplasmin ; physiology ; Female ; Ferritins ; physiology ; Hemochromatosis Protein ; Hepcidins ; Histocompatibility Antigens Class I ; physiology ; Humans ; Iron ; metabolism ; Iron-Regulatory Proteins ; physiology ; Membrane Proteins ; physiology ; Placenta ; metabolism ; Pregnancy ; Transferrin ; physiology

AIMTo observe the effects of different periods of exercise on the iron status.

METHODSFemale rats were randomly divided into 3-, 6-, 12-month swimming exercise groups and their corresponding sedentary groups. The hematological indices of iron status and the non-heme iron (NHI) and total NHI (TNHI) of the organs were determined at the end of the desired period.

RESULTSAs compared with the corresponding sedentary groups, plasma iron and transferrin-iron saturation of three exercise groups were decreased without significant changes of blood hemoglobin and hematocrit. The NHI contents and TNHI of the liver, spleen and kidney were decreased. Although the NHI contents of the heart decreased, TNHI was not significantly changed. TNHI of the organs in both the exercised and sedentary rats were found to increase with age.

CONCLUSIONThe exercise-induced low iron status with depleted iron storage is similar to the iron-deficiency status, but it could not be explained using the hypothesis of iron deficiency. Both the NHI redistribution and the maintained iron storage suggests the adaptation of low iron status to exercise. Therefore, the so-called exercise-induced iron deficiency could not exist.

Animals ; Female ; Hematocrit ; Iron ; deficiency ; metabolism ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Sprague-Dawley ; Swimming ; physiology

BACKGROUNDAlthough there are several drugs and drug combinations for the treatment of Pneumocystis carinii (P. carinii) pneumonia, all drugs have the toxicity as well as low efficacy. Iron chelators have been proposed as a source of new drugs for combating these infections. We hypothesized that iron chelators would suppress the growth of P. carinii by deprivation of the nutritional iron required for growth. In this study, a short-term axenic culture system of P. carinii was established. Daphnetin (7,8-dihydroxycoumarin), a known iron chelator, was demonstrated to exhibit in vitro activity against P. carinii in this system.

METHODSP. carinii organisms were obtained from the lungs of immunosuppressed rats. The culture system consisted of Iscove Dulbecco Eagle's Minimum Essential Medium (IMDM), supplemented with S-adenosyl-L-methionine, N-acetylglucosamine, putrescine, L-cysteine, L-glutamine, 2-mercaptoethanol, and fetal bovine serum, and was maintained at 37 degrees C, in 5% CO(2), 95% O(2), at the optimal pH of 8.0. The culture system was used to assess the effect of daphnetin on the proliferation of P. carinii organisms. The ultrastructures of the treated organisms were observed by transmission electron microscopy.

RESULTSThe number of cysts and trophozoites increased 8- to 9-fold and 11- to 12-fold, respectively, after 10 days of culture. Daphnetin was found to suppress the growth of P. carinii in a dose-dependent manner at concentrations between 1 micromol/L and 20 micromol/L. The inhibitory activity was suppressed by the chelation of daphnetin with ferrous sulfate in a 2:1 molar ratio, but it was not suppressed by mixing the culture medium with magnesium sulfate. Reduction of P. carinii numbers after treatment with daphnetin correlated with morphological changes in the organisms, as determined by transmission electron microscopy.

CONCLUSIONSDaphnetin can suppress the growth of P. carinii in vitro. The efficacy of daphnetin in suppressing the the growth of P. carinii in vitro is related to its ability to chelate iron.

Iron ; physiology ; Iron Chelating Agents ; pharmacology ; Microscopy, Electron ; Pneumocystis carinii ; drug effects ; growth & development ; ultrastructure ; Umbelliferones ; pharmacology

Accumulating evidence has revealed that brain iron concentrations increase with aging, and the choroid plexus (CP) may be at the basis of iron-mediated toxicity and the increase in inflammation and oxidative stress that occurs with aging. The mechanism involves not only hepcidin, the key hormone in iron metabolism, but also iron-related proteins and signaling-transduction molecules, such as IL-6 and signal transducer and activator of transcription 3 (Stat3). The aim of the present study was to investigate the correlation between the IL-6/Stat3 signaling pathway and hepcidin at the CP in normal aging. Quantitative real time PCR and Western blot were used to determine the alterations in specific mRNA and corresponding protein changes at the CP at ages of 3, 6, 9, 12, 15, 18, 21, 24, 27, 30, 33 and 36 months in Brown-Norway/Fischer (B-N/F) rats. The results demonstrated that hepcidin mRNA level at the CP kept stable in young rats (from 3 to 18 months), and increased with aging (from 21 to 36 months). The alterations of IL-6/p-Stat3 mRNA and protein expressions in normal aging were in accordance with that of hepcidin mRNA. Our data suggest that IL-6 may regulate hepcidin expression at the CP, upon interaction with the cognate cellular receptor, and through the Stat3 signaling transduction pathway.
Aging ; physiology ; Animals ; Choroid Plexus ; metabolism ; Hepcidins ; physiology ; Interleukin-6 ; physiology ; Iron ; metabolism ; RNA, Messenger ; Rats ; Rats, Inbred F344 ; STAT3 Transcription Factor ; physiology ; Signal Transduction

OBJECTIVETo investigate the effects of long time cruising on fishermen' immune function and nutrition state.

METHODSThirty-two fishermen's lymphocyte subsets, immunoglobulin, alexin, prealbumin, albumin, blood fat, hemoglobin serum iron, transferrin were tested before and after cruising.

RESULTSThe expression of CD-19 was significantly higher after cruising (P < 0.001) while other cell immune functions were not significantly changed. After cruising, the immunoglobulin IgG, IgA, alexin C3, B, prealbumin, albumin, transferrin were higher than before cruising (P < 0.001). HDL-C was higher (P < 0.05); Apo-B, and serum iron were lower (P < 0.01).

CONCLUSIONThe cruising fishermen' immune function is changed significantly; the nutrition state is good, but the serum iron is insufficient and in subclinical state.

Adult ; Fisheries ; Humans ; Immune System ; physiology ; Iron ; deficiency ; Male ; Nutrition Surveys ; Nutritional Status

Hepcidin is a small cystein-rich cationic peptide produced mainly by the liver. It was initially isolated from human plasma and exhibited antimicrobial activity. Recently, several lines of evidence have suggested that hepcidin is a key regulator of iron metabolism at the whole body level and is relative to inflammation, infection, hypoxia and anemia. Hepcidin, is implicated in duodenal iron absorption and iron mobilization from reticuloendothelial macrophages. The major mechanism of hepcidin function seems to be the regulation of transmembrane iron transport. As both iron deficiency and iron excess are associated with cellular dysfunction, so hepcidin or hepcidin-related therapeutics could find a place in the treatment of various diseases such as hemochromatosis and anemia of chronic disease. To elucidate biological function of hepcidin further and use it for other research, it is necessary to produce enough hepcidin through DNA recombinant technique. As a highly successful system for the production of a variety of heterologous proteins, the methylotrophic Pichia pastoris system has the probability for a high level production of hepcidin. The subject of this paper is to summarize the regulation of hepcidin gene expression and the understanding of functions of hepcidin. At last, giving a prospect of production hepcidin by gene engineer.
Antimicrobial Cationic Peptides ; biosynthesis ; genetics ; physiology ; Hepcidins ; Humans ; Iron ; metabolism ; Protein Engineering ; methods

Ferroptosis is a type of regulated cell death driven by iron-dependent lipid peroxidation that has received extensive attention in recent years. A growing body of evidence suggests that ferroptosis contributes to the progression of drug-induced liver injury. Therefore, the role and mechanism of ferroptosis in the process of drug-induced liver injury deserve further extensive and in-depth exploration, which will aid in the discovery of novel biomarkers as well as the identification of potential approches of targeting ferroptosis to intervene in drug-induced liver injury.
Humans ; Biomarkers/metabolism* ; Chemical and Drug Induced Liver Injury ; Ferroptosis ; Iron/metabolism* ; Lipid Peroxidation/physiology*

OBJECTIVEPrevious work has showed that excess iron accumulation is harmful to reproduction and even promotes death; however, whether the multiple biological toxicity of iron (Fe) exposure could be transferred to progeny remains unknown. The present study used Caenorhabditis elegans to analyze the multiple toxicities of iron exposure and their possible transferable properties.

METHODSThree concentrations of iron sulfate solution (2.5 micromol/L, 75 micromol/L, and 200 micromol/L) were used. The endpoints of lifespan, body size, generation time, brood size, head thrash and body bend frequencies, and chemotaxis plasticity were selected to investigate Fe toxicity and its effect on progeny in Caenorhabditis elegans.

RESULTSThe Fe toxicity could cause multiple biological defects in a dose-dependent manner by affecting different endpoints in nematodes. Most of the multiple biological defects and behavior toxicities could be transferred from Fe-exposed Caenorhabditis elegans to their progeny. Compared to the parents, no recovery phenotypes were observed for some of the defects in the progeny, such as body bend frequency and life span. We further summarized the defects caused by Fe exposure into 2 groups according to their transferable properties.

CONCLUSIONOur results suggest that Fe exposure could cause multiple biological defects, and most of these severe defects could be transferred from Fe exposed nematodes to their progeny.

Animals ; Behavior, Animal ; drug effects ; physiology ; Body Size ; Caenorhabditis elegans ; drug effects ; genetics ; physiology ; Dose-Response Relationship, Drug ; Iron ; toxicity ; Iron Compounds ; toxicity ; Life Expectancy ; Phenotype ; Reproduction ; Soil Pollutants ; toxicity ; Sulfates ; toxicity