ascorbic-acid and ferric-sulfate

The aim of this study was to determine whether iron deficiency anemia (IDA) in mothers alters their maternal cognitive and behavioral performance, the mother-infant interaction, and the infant's development. This article focuses on the relation between IDA and cognition as well as behavioral affect in the young mothers. This prospective, randomized, controlled, intervention trial was conducted in South Africa among 3 groups of mothers: nonanemic controls and anemic mothers receiving either placebo (10 microg folate and 25 mg vitamin C) or daily iron (125 mg FeS0(4), 10 microg folate, 25 mg vitamin C). Mothers of full-term normal birth weight babies were followed from 10 wk to 9 mo postpartum (n = 81). Maternal hematologic and iron status, socioeconomic, cognitive, and emotional status, mother-infant interaction, and the development of the infants were assessed at 10 wk and 9 mo postpartum. Behavioral and cognitive variables at baseline did not differ between iron-deficient anemic mothers and nonanemic mothers. However, iron treatment resulted in a 25% improvement (P < 0.05) in previously iron-deficient mothers' depression and stress scales as well as in the Raven's Progressive Matrices test. Anemic mothers administered placebo did not improve in behavioral measures. Multivariate analysis showed a strong association between iron status variables (hemoglobin, mean corpuscular volume, and transferrin saturation) and cognitive variables (Digit Symbol) as well as behavioral variables (anxiety, stress, depression). This study demonstrates that there is a strong relation between iron status and depression, stress, and cognitive functioning in poor African mothers during the postpartum period. There are likely ramifications of this poorer "functioning" on mother-child interactions and infant development, but the constraints around this relation will have to be defined in larger studies.

Topics: Adult; Anemia, Iron-Deficiency; Ascorbic Acid; Cognition; Demography; Depression; Dietary Supplements; Educational Status; Emotions; Female; Ferric Compounds; Humans; Income; Placebos; Pregnancy; Pregnancy Complications; Puerperal Disorders; South Africa; Stress, Psychological

The potential use of an extrinsic label to measure iron absorption from a ferric orthophosphate-fortified malted cocoa drink was examined by measuring the solubility of the FePO4 in 0.1 M-hydrochloric acid. The validity of using the stable isotope 58Fe as an extrinsic label was tested by comparing Fe absorption by rats from wheat flour extrinsically-labelled with 58Fe or 59Fe. Fe absorption from a malted cocoa drink (20 g powder made up with hot water) fortified with FePO4 (0.5 mg Fe/g powder) was measured in human subjects using 58Fe as an extrinsic label. Absorption was calculated by measuring unabsorbed 58Fe in faeces. Absorptions of Fe from the drink fortified with either FePO4 or ferrous sulphate were compared. The effect of the addition of ascorbic acid to the drink (1 mg/g powder) on Fe availability was also examined. The effect of fasting on Fe absorption from the drink was determined in rats by giving the drink to fasting animals or shortly after they had consumed a small meal. The FePO4 was totally soluble in 0.1 M-HCl and there were no differences in absorption between 58Fe- and 59Fe-labelled wheat flour. In the human experiment the proportion of Fe absorbed from the drink plus FePO4 and ascorbic acid was (mean with SE) 0.25 (0.02), from the drink plus FePO4 0.24 (0.02) and from the drink plus FeSO4 0.23 (0.03). Fasting had a significant effect on Fe availability; rats given the drink shortly after a small meal absorbed less than half as much Fe as those given the drink on a fasted stomach. It was concluded that the FePO4 used to fortify the malted cocoa drink was as well absorbed as FeSO4 but that the high levels of absorption were a reflection of the fasting condition of the subjects. The level of ascorbic acid was not great enough to enhance the availability of the FePO4 any further.

Topics: Adult; Animals; Ascorbic Acid; Beverages; Cacao; Edible Grain; Fasting; Ferric Compounds; Humans; Intestinal Absorption; Iron; Iron Isotopes; Male; Radioisotopes; Rats; Rats, Inbred Strains

Topics: Acrylamides; Administration, Oral; Anemia; Ascorbic Acid; Caco-2 Cells; Cell Survival; Drug Carriers; Drug Delivery Systems; Ferric Compounds; Ferritins; Heme; Hemin; Humans; Hydrogen-Ion Concentration; Iron; Micelles; Microscopy, Confocal; Molecular Weight; Particle Size; Polyethylene Glycols; Polymers; Sulfates; Temperature; Ultraviolet Rays

Interaction between Vitamin C (VitC) and transition metals can induce the formation of reactive oxygen species (ROS). VitC may also act as an ROS scavenger and as a metal chelant. To examine these possibilities, we tested in vivo the effect of two doses of VitC (1 and 30 mg/kg of mouse body weight) on the genotoxicity of known mutagens and transition metals. We used the alkaline version of the comet assay to assess DNA damage in peripheral white blood cells of mice. Animals were orally given either water (control), cyclophosphamide (CP), methyl methanesulfonate (MMS), cupric sulfate or ferrous sulfate. A single treatment with each VitC dose was administered after treatment with the mutagens or the metal sulfates. Both doses of VitC enhanced DNA damage caused by the metal sulfates. DNA damage caused by MMS was significantly reduced by the lower dose, but not by the higher dose of VitC. For CP, neither post-treatment dose of VitC affected the DNA damage level. These results indicate a modulatory role of Vitamin C in the genotoxicity/repair effect of these compounds. Single treatment with either dose of VitC showed genotoxic effects after 24 h but not after 48 h, indicating repair. Double treatment with VitC (at 0 and 24 h) induced a cumulative genotoxic response at 48 h, more intense for the higher dose. The results suggest that VitC can be either genotoxic or a repair stimulant, since the alkaline version of the comet assay does not differentiate "effective" strand breaks from those generated as an intermediate step in excision repair (incomplete excision repair sites). Further data is needed to shed light upon the beneficial/noxious effects of VitC.

Topics: Animals; Antineoplastic Agents, Alkylating; Antioxidants; Ascorbic Acid; Comet Assay; Copper Sulfate; Cyclophosphamide; DNA Damage; DNA Repair; Emetics; Ferric Compounds; Free Radical Scavengers; Leukocytes; Male; Methyl Methanesulfonate; Mice; Reactive Oxygen Species

Fenton's destruction of benzene, toluene, ethylbenzene, and xylene (BTEX) was investigated in soil slurry batch reactors. The purpose of the investigation was to quantify the enhancement of oxidation rates and efficiency by varying process conditions such as iron catalyst (Fe(II) or Fe(III); 2, 5, and 10mM), hydrogen peroxide (H2O2; 30, 150, 300 mM), and metal chelating agents (l-ascorbic acid, gallic acid, or N-(2-hydroxyethyl)iminodiacetic acid). Rapid contaminant mass destruction (97% after 3h) occurred in the presence of 300 mM H2O2 and 10 mM Fe(III). An enhanced removal rate (>90% removal after 15 min and 95% removal after 3h) was also observed by combining Fe(III), N-(2-hydroxyethyl)iminodiacetic acid and 300 mM H2O2. The observed BTEX mass removal rate constants (3.6-7.8 x 10(-4)s(-1)) were compared to the estimated rate constants (4.1-10.1 x 10(-3)s(-1)). The influence of non-specific oxidants loss (by reaction with iron hydroxides and soil organic matter) was also explored.

Topics: Ascorbic Acid; Catalysis; Chelating Agents; Ferric Compounds; Ferrous Compounds; Gallic Acid; Hydrocarbons, Aromatic; Hydrogen Peroxide; Imino Acids; Kinetics; Models, Chemical; Oxidation-Reduction; Soil Pollutants; Waste Management

SOS chromotest was employed to study the interaction of ascorbic acid with free ions of transient metals in the presence of added catalase, superoxide dismutase or D-mannitol. Catalase diminished the genotoxic activity of the mixture of ascorbic acid with copper ions in E. coli strains PQ37 and PQ 300, but genotoxicity of this mixture was not suppressed by superoxide dismutase and D-mannitol. The results suggest that copper ions diminished the content of peroxide generated by ascorbic acid.

Topics: Antioxidants; Ascorbic Acid; Catalase; Copper; Drug Interactions; Escherichia coli; Ferric Compounds; Free Radical Scavengers; Mannitol; Mutagens; Oxidation-Reduction; Reactive Oxygen Species; SOS Response, Genetics; Superoxide Dismutase

Activated pancreatic stellate cells have recently been implicated in pancreatic fibrogenesis. This study examined the role of pancreatic stellate cells in alcoholic pancreatic fibrosis by determining whether these cells are activated by ethanol itself and, if so, whether such activation is caused by the metabolism of ethanol to acetaldehyde and/or the generation of oxidant stress within the cells.. Cultured rat pancreatic stellate cells were incubated with ethanol or acetaldehyde. Activation was assessed by cell proliferation, alpha-smooth muscle actin expression, and collagen synthesis. Alcohol dehydrogenase (ADH) activity in stellate cells and the influence of the ADH inhibitor 4-methylpyrazole (4MP) on the response of these cells to ethanol was assessed. Malondialdehyde levels were determined as an indicator of lipid peroxidation. The effect of the antioxidant vitamin E on the response of stellate cells to ethanol or acetaldehyde was also examined.. Exposure to ethanol or acetaldehyde led to cell activation and intracellular lipid peroxidation. These changes were prevented by the antioxidant vitamin E. Stellate cells exhibited ethanol-inducible ADH activity. Inhibition of ADH by 4MP prevented ethanol-induced cell activation.. Pancreatic stellate cells are activated on exposure to ethanol. This effect of ethanol is most likely mediated by its metabolism (via ADH) to acetaldehyde and the generation of oxidant stress within the cells.

Topics: Acetaldehyde; Actins; Animals; Ascorbic Acid; Cell Division; Cells, Cultured; Collagen; Drug Combinations; Ethanol; Ferric Compounds; Fibrosis; Lipid Peroxides; Malondialdehyde; Muscle, Smooth; Oxidative Stress; Pancreas; Rats

Reactive oxygen and nitrogen species (RO/NS) such as nitric oxide (NO), hydroxyl radical (OH.), and superoxide anion (O(2)(-)) are generated in a variety of neuropathological processes and damage neurons. In the present study, we investigated the neuroprotective effects of rat astrocytes against RO/NS-induced damage using neuron-glia cocultures, and the effects were compared to those of microglial cells. Sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1), and FeSO(4) were used to generate NO, O(2)(-) and NO, and OH., respectively. Solely cultured neurons, which were transiently exposed to these agents, degenerated, possibly through apoptotic mechanisms as revealed by in situ detection of DNA fragmentation, whereas neurons cocultured with either astrocytes or microglial cells were viable even after exposure to RO/NS. In contrast, most neurons cocultured with meningeal fibroblasts degenerated. Astrocyte-conditioned medium partially attenuated RO/NS-induced neuronal damage. When neurons were cultured on astrocyte-derived extracellular matrix (AsECM), neuronal death induced by SNP and FeSO(4) was almost completely inhibited. AsECM contained significant amounts of laminin and fibronectin, and pure fibronectin and laminin also protected neurons against RO/NS-induced damage in the same manner as AsECM. These results suggest that astrocytes can protect neurons against RO/NS-induced damage by secreting soluble and insoluble factors.

Topics: Animals; Ascorbic Acid; Astrocytes; Cell Culture Techniques; Cell Death; Coloring Agents; Extracellular Matrix; Ferric Compounds; Fibronectins; Free Radical Scavengers; Hydroxyl Radical; Immunoblotting; Immunohistochemistry; In Situ Nick-End Labeling; Indicators and Reagents; Laminin; Microtubule-Associated Proteins; Molsidomine; Neurons; Nitric Oxide; Nitric Oxide Donors; Nitroprusside; Oxazines; Oxidative Stress; Rats; Reactive Oxygen Species; Xanthenes

Human ether-a-gogo related gene (HERG) K+ channels are key elements in the control of cell excitability in both the cardiovascular and the central nervous systems. For this reason, the possible modulation by reactive oxygen species (ROS) of HERG and other cloned K+ channels expressed in Xenopus oocytes has been explored in the present study. Exposure of Xenopus oocytes to an extracellular solution containing FeSO4 (25-100 microM) and ascorbic acid (50-200 microM) (Fe/Asc) increased both malondialdehyde content and 2',7'-dichlorofluorescin fluorescence, two indexes of ROS production. Oocyte perfusion with Fe/Asc caused a 50% increase of the outward K+ currents carried by HERG channels, whereas inward currents were not modified. This ROS-induced increase in HERG outward K+ currents was due to a depolarizing shift of the voltage-dependence of channel inactivation, with no change in channel activation. No effect of Fe/Asc was observed on the expressed K+ currents carried by other K+ channels such as bEAG, rDRK1, and mIRK1. Fe/Asc-induced stimulation of HERG outward currents was completely prevented by perfusion of the oocytes with a ROS scavenger mixture (containing 1,000 units/ml catalase, 200 ng/ml superoxide dismutase, and 2 mM mannitol). Furthermore, the scavenger mixture also was able to reduce HERG outward currents in resting conditions by 30%, an effect mimicked by catalase alone. In conclusion, the present results seem to suggest that changes in ROS production can specifically influence K+ currents carried by the HERG channels.

Topics: Animals; Ascorbic Acid; Cation Transport Proteins; Cloning, Molecular; DNA-Binding Proteins; ERG1 Potassium Channel; Ether-A-Go-Go Potassium Channels; Female; Ferric Compounds; Free Radical Scavengers; Humans; Kinetics; Malondialdehyde; Membrane Potentials; Oocytes; Potassium Channels; Potassium Channels, Voltage-Gated; Reactive Oxygen Species; Recombinant Proteins; Trans-Activators; Transcriptional Regulator ERG; Xenopus

In this study, the protective effect of melatonin against kainate (KA)-induced neurotoxicity was evaluated in vitro and in vivo. In rat brain synaptosomes, KA-induced oxidative stress was measured as shown by significant increases in both the basal generation of reactive oxygen species (ROS), assessed by a fluorescent method, and lipid peroxidation, evaluated as malondialdehyde (MDA) levels. Melatonin decreased, in a concentration-dependent manner, KA-induced lipid peroxidation. The intrinsic fluorescence of melatonin molecule hindered the evaluation of its protective effect against KA-induced ROS generation. However, melatonin was able to reduce FeSO4/ascorbate-induced ROS generation. The melatonin protective effect was confirmed by in vivo experiments: 73% of rats injected with KA (10 mg/kg i.p.) died within 5 days; melatonin administration i.p. significantly reduced mortality of the animals. The present results suggest that melatonin might be considered a pharmacological agent for the treatment of neurodegenerative pathologies.

Topics: Animals; Ascorbic Acid; Brain; Brain Diseases; Dose-Response Relationship, Drug; Ferric Compounds; Kainic Acid; Lipid Peroxidation; Male; Melatonin; Oxidative Stress; Rats; Rats, Wistar; Reactive Oxygen Species; Synaptosomes

Various small oxidation products (e.g. 8-hydroxydeoxyguanosine) can be induced in DNA by nickel compounds. In this study, the 32P-postlabeling assay was applied to determine whether Ni(II) compounds are able to induce bulky DNA-adduct formation in vitro and in vivo. In vitro studies detected two major and several minor adducts in DNA incubated with NiCl2 and H2O2 at 37 degrees C for 1 h. Formation of the two major adducts increased with incubation time (0-24 h) and NiCl2 concentration (0-800 microM). Adduct levels were greatly reduced by hydroxyl free-radical scavengers, i.e. 0.4 M sodium formate or 0.05 M p-nitrosodimethylaniline, and by a singlet oxygen scavenger, 0.05 M sodium azide. The in vitro effects of NiCl2 on DNA were significantly enhanced by (1) addition of 3 mM ascorbic acid, (2) replacement of H2O with D2O in the reaction, and (3) prior denaturation of DNA. Adduct formation presumably involved a Fenton-type reaction, in which DNA crosslinks may arise by reaction with hydroxyl free radicals and singlet oxygen. For in vivo studies, male 6-8 wk old B6C3F1 mice were used. In untreated mice, several I-compounds (putative indigenous DNA modifications that increase with age) were detected in liver, kidney, and lung. Two of these (spots 1 and 2) were chromatographically identical to the two major spots induced by Ni(II) in vitro. The intensities of spots 1 and 2 in kidney and of some other spots in liver and lung were increased 1 and 2 h after i.p. injection with a single dose of 170 mumols/kg NiAc2. The effects of NiAc2 were reduced or undetectable in the three tissues 24 h after treatment. These observations indicate the capacity of Ni(II) to induce and modulate bulky DNA modifications both in vitro and in vivo.

Topics: Animals; Ascorbic Acid; Carcinogenicity Tests; Chromatography, Thin Layer; Deuterium; Deuterium Oxide; DNA; Ferric Compounds; Free Radical Scavengers; Kidney; Liver; Lung; Male; Mice; Mice, Inbred Strains; Mutagens; Nickel; Phosphorus Isotopes; Reactive Oxygen Species; Water

Iron is believed to contribute to the process of cell damage and death resulting from ischemic and traumatic insults by catalyzing the oxidation of protein and lipids. Exposure of cultured rat hippocampal neurons to iron (FeSO4) caused a dose-dependent reduction in neuronal survival, which was potentiated by ascorbate. Damage to neurons was associated with a significant level of oxygen radical in the culture medium. The iron chelator desferal prevented both the neuronal degeneration caused by FeSO4 and the production of oxygen radical, demonstrating that ionic iron was responsible for the cell damage. Iron neurotoxicity was associated with an elevation of [Ca2+]i and was attenuated by NMDA receptor antagonists. Since recent findings demonstrated neuroprotective effects of growth factors in cell culture and in vivo models of ischemia, we examined the effects of growth factors on iron-induced damage. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and insulin-like growth factors (IGF-I and IGF-II) each protected neurons against iron-induced damage. Both rat hippocampal and human cortical neurons were protected by these growth factors. Taken together, the data suggest that the neuroprotective effects of growth factors against excitotoxic/ischemic insults may result, in part, from a prevention or attenuation of oxidative damage.

Topics: Animals; Ascorbic Acid; Calcium; Cerebral Cortex; Ferric Compounds; Fibroblast Growth Factor 2; Growth Substances; Hippocampus; Iron; Nerve Growth Factors; Neurons; Receptors, N-Methyl-D-Aspartate; Somatomedins

Oxygen free radicals generated by the interaction of Fe2+ and H2O2 (Fenton reaction) are capable of reacting with DNA bases, which may induce premutagenic and precarcinogenic lesions. Products formed in DNA by such reactions have been characterized as hydroxylated derivatives of cytosine, thymine, adenine, and guanine and imidazole ring-opened derivatives of adenine and guanine. As shown here by 32P-postlabeling, incubation of DNA under Fenton reaction conditions gave rise to additional oxidation products in DNA that were characterized as putative ribonucleosides by enzymatic hydrolysis of the oxidized DNA, 32P-postlabeling, and co-chromatography in multiple systems with authentic markers. Formation of these products in DNA was enhanced by the presence of L-ascorbic acid in the reaction mixtures and their total amounts were similar to those of the major DNA oxidation product, 8-hydroxy-2'-deoxyguanosine. The ribonucleoside guanosine was also formed in kidney DNA of male rats treated with ferric nitrilotriacetate, a renal carcinogen. It is postulated that ribonucleotides alter conformation and function of DNA and thus their presence in DNA may lead to adverse health effects.

Topics: Adenosine Triphosphate; Animals; Ascorbic Acid; Chromatography, Thin Layer; DNA; DNA Damage; Female; Ferric Compounds; Free Radicals; Hydrogen Peroxide; Hydroxylation; Male; Oxidation-Reduction; Phosphorus Radioisotopes; Radioisotope Dilution Technique; Rats; Rats, Inbred F344; Rats, Sprague-Dawley; Ribonucleosides; Ribonucleotides

The possible role of lipid peroxidation in the nephrotoxicity of the antitumour drug cisplatin was studied in vitro. In contrast to Adriamycin, cisplatin did not induce lipid peroxidation in rat kidney microsomes containing a NADPH-generating system. Pretreatment of rat kidney microsomes with cisplatin did not reduce the activity of a microsomal glutathione (GSH)-dependent protective factor against lipid peroxidation induced by Fe(2+)-ascorbate. However, pretreatment of rat kidney microsomes with 0.1 mM N-ethyl maleimide (NEM) did reduce this GSH-dependent protection. Cisplatin also did not reduce the activity of a cytosolic GSH-dependent protective factor against Fe(2+)-ascorbate-induced lipid peroxidation. The results of our experiments indicate that, in contrast to Adriamycin, cisplatin does not induce lipid peroxidation in vitro in various test systems. It also does not destroy microsomal and cytosolic GSH-dependent protective factors against lipid peroxidation.

Topics: Animals; Ascorbic Acid; Cisplatin; Cytosol; Doxorubicin; Ferric Compounds; Hot Temperature; Kidney; Lipid Peroxidation; Male; Microsomes; NADP; Rats; Rats, Wistar; Thiobarbiturates

Hydrogen peroxide inactivates the purified human angiotensin-converting enzyme (ACE) in vitro; the inactivating effect of H2O2 is eliminated by an addition of catalase. The lung and kidney ACE are equally sensitive to the effect of hydrogen peroxide. After addition of oxidants (H2O2 alone or H2O2 + ascorbate or H2O2 + Fe2+ mixtures) to the membranes or homogenates of the lung, the inactivation of membrane-bound ACE is far less pronounced despite the large-scale accumulation of lipid peroxidation products. The marked inactivation of ACE in the membrane fraction (up to 55% of original activity) was observed during ACE incubation with a glucose:glucose oxidase:Fe2+ mixture. Presumably the oxidative potential of H2O2 in tissues in consumed, predominantly, for the oxidation of other components of the membrane (e.g., lipids) rather than for ACE inactivation.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antibodies, Monoclonal; Ascorbic Acid; Catalase; Ferric Compounds; Humans; Hydrogen Peroxide; Lung; Oxidation-Reduction; Peptidyl-Dipeptidase A; Rats; Spectrometry, Fluorescence

The relation between cerebral oxygen radicals and the aging process was investigated in crude synaptosomal (P2) fractions from rats. The rate of formation of oxygen radicals was measured using the probe 2',7'-dichlorofluorescein diacetate (DCFH-DA), which is de-esterified and subsequently oxidized by oxygen radicals to a fluorescent product 2',7'-dichlorofluorescein (DCF). There was a significant age-dependent decrease in the formation rate of oxygen radicals, observed by decreased formation of DCF. No difference in oxygen radical formation was apparent between age groups following an in vitro challenge with an ascorbate/FeSO4 mixture. This age-dependent decrease in cerebral oxygen radical generation coincided with age-dependent increases in superoxide dismutase. No age-related alterations in lipid order in either the hydrophilic or lipophilic membrane regions were observed using fluorescence polarization analysis. Age-dependent losses in cerebral P2 tryptophan fluorescence (a measure of protein degradation), and increased liberation of [14C]protein fragments into the acid-soluble fraction (a measure of overall proteolytic activity) were observed. Results suggest that aging does not proceed as a result of elevated rates of generation of oxygen radicals, a finding that does not support the proposed free radical theory of aging. The observed age-dependent decrease in the formation of oxygen radicals does not effect membrane lipid order. These findings implicate modifications in proteins and activated protein catabolic pathways as major contributing factors in the normal physiological process of senescence.

Topics: Aging; Animals; Ascorbic Acid; Brain; Cerebral Cortex; Ferric Compounds; Fluoresceins; Free Radicals; In Vitro Techniques; Male; Nerve Tissue Proteins; Oxygen Consumption; Rats; Rats, Inbred F344; Superoxide Dismutase; Tryptophan

Consumption of edible oils contaminated with Argemone mexicana seed oil causes various toxic manifestations. In this investigation the in vivo effect of argemone oil on NADPH-dependent enzymatic and Fe2+-, Fe2+/ADP- or ascorbic acid-dependent non-enzymatic hepato-subcellular lipid peroxidation was studied. Parenteral administration of argemone oil (5 ml/kg body weight) daily for 3 days produced a significant increase in both non-enzymatic and NADPH-supported enzymatic lipid peroxidation in whole homogenate, mitochondria, and microsomes. Lipid peroxidation aided by various pro-oxidants, namely Fe2+, Fe2+/ADP and ascorbic acid also revealed a significant enhancement in the whole homogenate, mitochondria and microsomes of argemone oil-treated rats. Further, when compared with whole homogenate, the hepatic mitochondria and microsomes of either control or argemone oil-treated rats showed a 4- and 6-fold increase in non-enzymatic, and a 5- and 18-fold increase in NADPH-dependent enzymatic lipid peroxidation, respectively. Similarly, both mitochondrial and microsomal fractions showed a 5- and 7-fold increase in Fe2+-, and a 12- and 15-fold increase in either Fe2+/ADP- or ascorbic acid-aided lipid peroxidation, respectively. These results suggest that the hepatic microsomal as well as the mitochondrial membrane is vulnerable to the peroxidative attack of argemone oil and may be instrumental in leading to the hepatotoxicity symptoms noted in argemone poisoning victims.

Topics: Animals; Ascorbic Acid; Dietary Fats; Ferric Compounds; Lipid Peroxides; Liver; Microsomes, Liver; Mitochondria, Liver; Plant Oils; Rats; Rats, Inbred Strains; Subcellular Fractions

Deoxyhypusine hydroxylase, the enzyme that catalyzes the formation of hypusine from deoxyhypusine in eukaryotic initiation factor 4D, has been partially purified from rat testis. The partially purified enzyme requires only the addition of certain sulfhydryl compounds for catalytic activity, dithiothreitol being the most effective. Its lack of dependency on the alpha-keto acid-dependent dioxygenase cofactors, Fe2+, alpha-ketoglutarate, and ascorbic acid, its failure to decarboxylate stoichiometrically alpha-ketoglutarate with deoxyhypusine hydroxylation, and its strong and specific inhibition by Fe2+ all suggest a catalytic mechanism of this enzyme unlike that of the prolyl and lysyl hydroxylases.

Topics: Animals; Ascorbic Acid; Chromatography, Gel; Cricetinae; Cricetulus; Dithiothreitol; Female; Ferric Compounds; Guinea Pigs; Ketoglutaric Acids; Kinetics; Male; Mixed Function Oxygenases; Ovary; Rabbits; Rats; Testis; Tissue Distribution

The significance of microsomal vitamin E in protecting against the free-radical process of lipid peroxidation was evaluated with the low-level-chemiluminescence technique in microsomal fractions from vitamin E-deficient and control rats. The induction period that normally precedes the ascorbate/ADP/Fe3+-induced lipid peroxidation was taken as reflecting the microsomal vitamin E content and was found to be 5-6-fold decreased in microsomal fractions from vitamin E-deficient rats. Supplementation of microsomal fractions from vitamin E-deficient rats with exogenous vitamin E partially restores the induction period observed in that from control rats. The decrease in chemiluminescence intensity and the increase in the induction period both correlate linearly with the amount of vitamin E added. However, the efficiency of exogenous vitamin E is about 50-fold lower than that exerted by the naturally occurring vitamin E in microsomal membranes. These observations are discussed in terms of the process of re-incorporation of vitamin E into membranes, the experimental model for lipid peroxidation selected, and the method to evaluate lipid peroxidation, namely low-level chemiluminescence.

Topics: Animals; Antioxidants; Ascorbic Acid; Ferric Compounds; In Vitro Techniques; Lipid Metabolism; Luminescent Measurements; Microsomes, Liver; Rats; Spectrophotometry; Vitamin E; Vitamin E Deficiency

Comparative study of isolated retinas of frogs and turtles exposed to rhythmical photostimulation was conducted. It was shown that there are marked differences between the responses of isolated retinas of frogs and turtles to the rhythmical photostimulation. A considerable depression of the total amplitude of the rhythmical electroretinogram was observed under the conditions of induced lipid peroxidation. Introduction of a selenium compound to the superfusing medium increased to a certain extent both the single and rhythmical responses of isolated retinas of the animals.

Topics: Animals; Ascorbic Acid; Electroretinography; Ferric Compounds; In Vitro Techniques; Lipid Peroxides; Periodicity; Photic Stimulation; Rana ridibunda; Retina; Selenious Acid; Selenium; Turtles; Vitamin E