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At least 919 records · Page 51Linked to original sources
PubMed2001

Potential of hemoglobin-based oxygen carriers in trauma patients.

Injured patients have a unique requirement for early blood transfusion. A product that can be used in the prehospital setting that adequately carries and delivers oxygen to peripheral tissues would potentially be life saving for severely injured patients. Allogeneic blood is not the ideal agent in the pre-hospital setting. Present limitations in the allogeneic blood supply include the need for cross-matching, refrigeration, marginal supply, transfusion reactions, infectious disease transmission and immunomodulation increasing the risk of organ dysfunction after transfusion.Hemoglobin-based oxygen carriers have been under present development for the last 25 years. These compounds use either human or bovine hemoglobin that is then chemically altered to improve safety. These compounds exhibit many desirable characteristics that make them potential therapeutic agents in the treatment of the injured patient. These compounds do not need to be cross-matched, have favorable oxygen dissociation characteristics, long half lives, do not transmit disease, appear to be less immunoreactive than blood and theoretically can be used in the pre-hospital setting as a low volume oxygen carrying solution without need for refrigeration. There are at least three agents presently under development that use different techniques to alter the basic hemoglobin tetramer. While there is no FDA approved hemoglobin-based oxygen carrier approved for use in injured patients at this writing, phase III studies are currently either underway or being developed. There is high likelihood that one or more of these agents will be approved for clinical use in the near future.

Aspirin↗
PubMed2000

Effects of selenium deficiency on the formation and detoxification of endogenous electrophiles in rats.

Selenium deficiency could be expected to lead to enhanced lipid peroxidation through loss of selenium-dependent glutathione peroxidase activity. Such a relation has, however, been difficult to verify. In the present study, the influence of selenium deficiency in rats on in vivo doses of some endogenously occurring low-molecular mass aldehydes and epoxides was determined. In vivo doses were measured by mass-spectrometric analysis according the N-alkyl Edman method of reaction products (adducts) with N-terminal valines in hemoglobin. Despite variations between experiments, the adduct levels of acetaldehyde and malonaldehyde were shown to be significantly higher in rats fed a selenium-deficient diet than in controls fed a selenium-adequate diet. No significant effect was found for the other aldehydes measured. In contrast, the in vivo doses of endogenous ethylene oxide and propylene oxide were lowered in selenium-deficient rats, indicating a 1.7-times faster detoxification rate. This was verified by the lower adduct levels in selenium-deficient rats following intraperitoneal administration of these epoxides at moderate doses. In conclusion, the results seem to reflect the complex changes of induced and reduced enzyme activities in response to selenium deficiency. Measurement of reactive compounds through their adducts to hemoglobin has shown its ability to elucidate the effects of selenium deficiency per se.

Journal Article↗
PubMed2002

Sickle cell disease--pathophysiology, clinical and diagnostic implications.

We review the current knowledge of the pathophysiology of sickle cell disease (SCD), the clinical complications and the state of the art in SCD diagnostics. Today, a flexible laboratory concept allows the fast and economic clarification of the patients' sickle cell hemoglobin (HbS) status, e.g. additional compound heterozygosities. In contrast to a well-investigated pathophysiology of the disease, factors influencing the severity of symptoms as well as some laboratory findings in SCD still lack a final explanation. In this review, we focus on red cell lysis resistance as an additional diagnostic tool in SCD. There is a need for further studies regarding lysis resistance in blood samples from patients with HbS.

Anemia, Sickle Cell↗
PubMedDate not supplied

Biotransformation of nitrosobenzene in the red cell and the role of glutathione.

1. In the red cell nitrosobenzene formed glutathione-sulphinanilide from reduced glutathione, and the corresponding sulphinanilide with the reactive cysteine residues of haemoglobin. 2. Glutathionesulphinanilide was reductively cleaved by an NADPH-linked reductase with formation of free analine half an equivalent of reduced glutathione and half of glutathione sulphinic acid. 3. About three quarters of the aniline produced from nitrosobenzene or phenylhydroxylamine was formed via this pathway within the red cell.

Aniline Compounds↗
PubMed1991

Does Tris-HCl effectively participate in transamination during hemoglobin pyridoxylation?

To test whether Tris is required for covalent binding of pyridoxal phosphate (PLP) to hemoglobin, we carried out the reaction in solutions of Tris homologues, carrying a blocked amine function. With the exception of Mono-Tris, these compounds permitted the synthesis of modified hemoglobins with acceptable spectral properties, P50 values, cooperativity and methemoglobin content, refuting Tris HCI participation during hemoglobin pyridoxylation.

Hemoglobins↗
PubMed1983

[Effects of 3 varieties of antisickling substances measured by ektacytometry as a function of oxygen pressure].

The ektacytometer measures with precision the deformability of erythrocytes during a continuous change in oxygen tension. Automation of the instrument renders easily feasible the evaluation of proposed antisickling compounds. Drugs representative of the three modes of action presently recognized have been selected: those which increase oxygen affinity (potassium cyanate); those which inhibit hemoglobin polymerization (butylurea); membrane-active compounds. An anionic phenothiazine (metiazinic acid) had an interesting activity on deformability.

Antisickling Agents↗
PubMed1988

Biomonitoring of aromatic amines II: Hemoglobin binding of some monocyclic aromatic amines.

Covalent binding of 13 monocyclic aromatic amines to hemoglobin was studied in female Wistar rats and hemoglobin binding indices were determined. The hemoglobin adducts were hydrolyzed under alkaline conditions. In all cases the parent amine could be identified by gas chromatography and with one exception represented the only cleavage product. The binding index varied considerably and was highest with p-chloroaniline (569) and lowest with 2,4,5-trimethylaniline (0.7). Five compounds were also studied in female B6C3F1 mice. Hemoglobin binding was lower than in rats, but to varying degrees. Hemoglobin binding correlated remarkably well with the maximum methemoglobin level achieved with the six examples studied. The results support the notion that the reaction of nitrosoarenes, as metabolites of arylamines, with hemoglobin represents a general pathway in vivo. The analysis of such hemoglobin adducts is recommended as a dosimeter in biological monitoring of humans in order to control exposure. It is too early, however, to assess the carcinogenic risk from hemoglobin binding data with these compounds.

Amines↗
PubMed2006

Expression of heat shock protein and hemoglobin genes in Chironomus tentans (Diptera, chironomidae) larvae exposed to various environmental pollutants: a potential biomarker of freshwater monitoring.

To identify a sensitive biomarker of freshwater monitoring, we evaluated pollutant-induced expression of heat shock proteins (HSPs) and hemoglobins (Hbs) genes in the larvae of the aquatic midge Chironomus tentans (Diptera, Chironomidae). As pollutants, we examined nonylphenol, bisphenol-A, 17alpha-ethynyl estradiol, bis(2-ethylhexyl) phthalate, endosulfan, paraquat dichloride, chloropyriphos, fenitrothion, cadmium chloride, lead nitrate, potassium dichromate, benzo[a]pyrene and carbon tetrachloride. We also investigated larval growth as a physiological descriptor by measuring changes in the body fresh weight and dry weight after chemical exposure. The response of the HSPs gene expression by chemical exposure was rapid and sensitive to low chemical concentrations but it was not stressor specific. Interestingly, an increase in the expression of HSPs genes was observed not only in a stress inducible form (HSP70), but also in a constitutively (HSC70) expressed form. The expression of Hb genes showed chemical-specific responses: that is, alkyl phenolic compounds increased the expression of hemoglobin genes, whereas pesticides decreased the expression. As expected, molecular-level markers were more sensitive than physiological endpoints, suggesting that gene expression could be developed as an early warning biomarker in this animal. The overall results suggest that the expression of HSP and Hb genes in Chironomus could give useful information for diagnosing general health conditions in fresh water ecosystem. The expression of Hb genes, in particular, seems to be a promising biomarker, especially in view of the potential of Chironomus larvae as a biomonitoring species and of the physiological particularities of their respiratory pigments.

Animals↗
PubMed1999

Hemoglobin and iron-evoked oxidative stress in the brain: protection by bile pigments, manganese and S-nitrosoglutathione.

In the present in vitro and in vivo study we investigated the pro-oxidant effects of hemoglobin, as well as the antioxidant effects of its metabolites, in the brain. Incubation of rat brain homogenates with hemoglobin (0-10 microM) but not hemin induced lipid peroxidation up to 24 h (EC50 = 1.2 microM). Hemoglobin's effects were similar to ferrous ion (EC50 = 1.7 microM) and were blocked by the chelating agent deferoxamine (IC50 0.5 microM) and a nitric oxide-releasing compound S-nitrosoglutathione (IC50 = 40 microM). However, metabolites of hemoglobin - biliverdin and bilirubin - inhibited brain lipid peroxidation induced by cell disruption and hemoglobin (biliverdin IC50 = 12-30 and bilirubin IC50 = 75-170 microM). Biliverdin's antioxidative effects in spontaneous and iron-evoked lipid peroxidation were further augmented by manganese (2 microM) since manganese is an antioxidative transition metal and conjugates with bile pigments. Intrastriatal infusion of hemoglobin (0-24 nmol) produced slight, but significant 20-22% decreases in striatal dopamine levels. Whereas, intrastriatal infusion of ferrous citrate (0-24 nmol) dose-dependently induced a greater 66% depletion of striatal dopamine which was preceded by an acute increase of lipid peroxidation. In conclusion, contrary to the in vitro results hemoglobin is far less neurotoxic than ferrous ions in the brain. It is speculated that hemoglobin may be partially detoxified by heme oxygenase and biliverdin reductase to its antioxidative metabolites in the brain. However, in head trauma and stroke, massive bleeding could significantly produce iron-mediated oxidative stress and neurodegeneration which could be minimized by endogenous antioxidants such as biliverdin, bilirubin, manganese and S-nitrosoglutathione.

Animals↗
PubMed1983

Alkylation of DNA and hemoglobin in the mouse following exposure to ethene and ethene oxide.

Exposure of mice to 14C-labelled ethene or ethene oxide gave rise to hydroxyethylations of nucleophilic sites in hemoglobin and DNA. The relative amounts of alkylation products of different amino acids in hemoglobin were the same for the two compounds. Furthermore, the ratio between the degree of alkylation of DNA in various organs and of hemoglobin was approximately the same, supporting a previous conclusion that ethene oxide is the reactive intermediate formed in vivo from ethene. A comparison of the degrees of alkylation obtained per unit exposure dose (ppm X h) of ethene oxide and of ethene, respectively, showed that at low levels of ethene about 8% of the inhaled amount is metabolized to ethene oxide. It was estimated that the maximal rate of metabolism (Vmax) of ethene corresponds to exposure to an air level of 4 ppm of ethene oxide.

Alkylation↗
PubMed1986

Sample pretreatment to minimize interferences from whole blood in the radioimmunoassay for cyclosporine.

There is much controversy as to whether the analysis of cyclosporine (CsA) should be performed by radioimmunoassay (RIA) or high-performance liquid chromatography (HPLC), and whether the specimen should be serum or whole blood. Whole-blood specimens present specific advantages, but the presence of hemoglobin (Hgb) and other endogenous compounds can produce major errors in the RIA by "quenching" the analytical signal or by interfering with the antigen-antibody binding in the assay. We have developed a simple pretreatment step to remove the Hgb and other proteins responsible for this error. Red cells in whole blood are hemolyzed with a mixture of acetonitrile and water, the protein precipitated with acetonitrile, and the supernatant assayed by RIA. In a controlled study in which CsA concentration was kept constant and the Hgb concentration varied, the errors in measurement were directly proportional (r = 0.999) to the Hgb concentration. CsA values were spuriously deflated or inflated by 22.7 micrograms/L for each gram per 100 milliliters that the Hgb deviated from the 9.2 g/100 ml Hgb in the CsA calibration standards. In a similar study in which patient samples (n = 57) were assayed with and without pretreatment, the fractional error induced by Hgb was compounded in some patients by additional interferences that also appear to be removed by sample pretreatment. Without the pretreatment, CsA values could be in error by 33% when the Hgb varied 4 g/100 ml, thus providing potentially misleading results to the clinician. An I-125-labeled CsA tracer (purported not to be affected by the "quenching" interference of Hgb) produced consistently higher results when it was substituted for the tritiated CsA tracer contained in the Sandoz kit. In summary, sample pretreatment appears to be the simplest method of effectively removing endogenous interferences and minimizing erroneous results from whole blood submitted to the Sandoz RIA for CsA analysis.

Chromatography, High Pressure Liquid↗