Hyaluronic Acid Degradation by Ascorbic Acid and Influence of Iron

The effects of ascorbic acid, iron and ADP on hyaluronic acid, a compound present in inflamed joints, were investigated in an in vitro system. Ascorbic acid induces degradation of hyaluronic acid which increased in the presence of FeCl, and which is additionally stimulated by ADP chelated ferric ions. The hyaluronic acid degrading reactions induced by the Fe-III/ADP/ascorbic acid system were inhibited by catalase and formate to various extents whereas the presence of superoxide dismutase did not exert any inhibitory effect. Desferrioxamine, a specific iron chelator, completely inhibited hyaluronic acid depolymerisation by ascorbic acid as well as in combination with FeCl₃ or FeCl₃/ADP, respectively. We suggest that the ultimate hyaluronic acid degrading species is OH', generated via the Fe-III/ADP catalysed Haber Weiss reaction. There is also an indication for the involvement of perferryl or/and ferryl species in the degradation process.     

Depolymerization of Hyaluronic Acid by Low-molecular-weight Amadori-rearrangement Products and Glycated Polylysine

Depolymerization of hyaluronic acid (HA) by low-molecular-weight Amadori-rearrangement products in the presence of Cu^{2 +} was studied as an in vitro model for the glycated protein-mediated degradation of biopolymers. This oxygen radical-mediated depolymerization was found to be specifically accelerated by Cu^{2 +} , and significantly inhibited by catalase, hydroxyl radical scavengers, and metal ion chelators. Glycated polylysine also depolymerized HA. The difference in depolymerization rate between low- and high-molecular-weight Amadori products is discussed.     

Depolymerization of Hyaluronic Acid by D-Fructose 6-Phosphate

Depolymerization of hyaluronic acid obtained from Streptococcus zooepidemicus by D-fructose 6-phosphate was investigated for characterization of reducing sugar-mediated degradation of biopolymers under physiological conditions. The extent of depolymerization was monitored by the decrease of viscosity of a reaction mixture containing 1.0% hyaluronic acid, D-fructose 6-phosphate, and 1.0 × 10^?2 mM of Cu²⁺ in phosphate buffer, pH 7.4. It was found that the depolymerization of hyaluronic acid was dependent on the concentration of the reducing sugar and was specifically accelerated by the presence of Cu²⁺. The reaction was found to be significantly inhibited by catalase, superoxide dismutase (SOD), 1,2-dihy­ droxybenzene 3,5-disulfonic acid (Tiron), and chelating agents such as EDTA and diethylene triamine penta­ acetic acid (DETAPAC), although the inhibition by SOD was low. Almost the same depolymerization rates were observed in hyaluronic acid preparations of different molecular weight (1.1 × 10⁶, 8.8 × 10⁵, and 6.8 × 10⁵). The rates, however, were different for hyaluronic acids obtained from S. zooepidemicus, rooster comb, and umbilical cord. It was concluded that depolymerization of the polysaccharide was caused by active oxygen species generated by the autoxidation of D-fructose 6-phosphate in the presence of Cu²⁺, in a mechanism similar to that previously reported for the degradation of DNA and inactivation of virus in vitro.     

Evaluation of the Antioxidant Actions of Ferulic Acid and Catechins

We have evaluated the abilities of ferulic acid, (±) catechin, (+) catechin and (-) epicatechin to scavenge the reactive oxygen species hydroxyl radical (OH±), hypochlorous acid (HOCl) and peroxyl radicals (RO₂).

Ferulic acid tested at concentrations up to 5 mM inhibited the peroxidation of phospholipid liposomes. Both (±) and (+) catechin and (-) epicatechin were much more effective. All the compounds tested reacted with trichloromethyl peroxyl radical (CCl₃O₂) with rate constants > 1 × 10⁶M^?1s^?1.

A mixture of FeCl₃-EDTA, hydrogen peroxide (H₂O₂) and ascorbic acid at pH 7.4, has often been used to generate hydroxyl radicals (OH.) which are detected by their ability to cause damage to the sugar deoxyribose. Ferulic acid, (+) and (±) catechin and (-) epicatechin inhibited deoxyribose damage by reacting with OH. with rate constants of 4.5 × 10⁹M^?1s^?1, 3.65 × 10⁹M^?1s^?1, 2.36 × 10⁹M^?1s^?1 and 2.84 × 10⁹M^?1s^?1 respectively. (-) Epicatechin, ferulic acid and the (+) and (±) catechins exerted pro-oxidant action, accelerating damage to DNA in the presence of a bleomycin-iron complex. On a molar basis, ferulic acid was less effective in causing damage to DNA compared with the catechins.

A mixture of hypoxanthine and xanthine oxidase generates O₂ which reduces cytochrome c to ferrocytochrome c. (+) Catechin and (-) epicatechin inhibited the reduction of cytochrome c in a concentration dependent manner. Ferulic acid and (±) catechin had only weak effects.

All the compounds tested were able to scavenge hypochlorous acid at a rate sufficient to protect alpha-1-antiproteinase against inactivation. Our results show that catechins and ferulic acid possess antioxidant properties. This may become important given the current search for “natural” replacements for synthetic antioxidant food additives.     

Iron prevents ascorbic acid (vitamin C) induced hydrogen peroxide accumulation in copper contaminated drinking water

Ascorbic acid (vitamin C) induced hydrogen peroxide (H₂O₂) formation was measured in household drinking water and metal supplemented Milli-Q water by using the FOX assay. Here we show that ascorbic acid readily induces H₂O₂ formation in Cu(II) supplemented Milli-Q water and poorly buffered household drinking water. In contrast to Cu(II), iron was not capable to support ascorbic acid induced H₂O₂ formation during acidic conditions (pH: 3.5–5). In 12 out of the 48 drinking water samples incubated with 2 mM ascorbic acid, the H₂O₂ concentration exceeded 400 μM. However, when trace amounts of Fe(III) (0.2 mg/l) was present during incubation, the ascorbic acid/Cu(II)-induced H₂O₂ accumulation was totally blocked. Of the other common divalent or trivalent metal ions tested, that are normally present in drinking water (calcium, magnesium, zinc, cobalt, manganese or aluminum), only calcium and magnesium displayed a modest inhibitory activity on the ascorbic acid/Cu(II)-induced H₂O₂ formation. Oxalic acid, one of the degradation products from ascorbic acid, was confirmed to actively participate in the iron induced degradation of H₂O₂. Ascorbic acid/Cu(II)-induced H₂O₂ formation during acidic conditions, as demonstrated here in poorly buffered drinking water, could be of importance in host defense against bacterial infections. In addition, our findings might explain the mechanism for the protective effect of iron against vitamin C induced cell toxicity.     

Leaching of iron and toxic heavy metals from anaerobically-digested sewage sludge

Summary Heavy metal-loaded sewage sludge was leached abiotically using FeCl₂ and FeCl₃ which are applied in waste water treatment plants to eliminate phosphate and for coagulation. Due to the hydrolyzing nature of ferric iron, ferric chloride (100 mmll L^–1) was able to solubilize more than 90% of copper and zinc and more than 80% of cadmium, with an optimal pulp density of 3% (w/v), after 10 h of exposition at 25°C. Chromium, lead and nickel were solubilized to an extent of 40–70%. With the exception of copper (redoxolysis), all heavy metals monitored were leached following the principle of acidolysis. Chemical leaching with iron resulted in a secondary contamination of sewage sludge (96 g iron per kg dry weight). The insoluble iron compounds which were precipitated for adsorbed to sludge flocks could be resolubilized with oxalic acid (100 mM, pH<3.3) up to an extent of 90%. Iron was leached by acidolysis and held in solution by complexation with oxalic acid. The pH optimum for the treatment of sewage sludge with 100 mmol L^–1 oxalic acid was pH 3.3. At this pH an excessive solubilization of nutrient elements and compounds (phosphorus, nitrogen, alkali and alkali earth elements) could be avoided concomitantly leaching 75% iron. Furthermore the hydrophobicity of the sewage sludge was significantly reduced as a result of treatment with iron chloride.Thiobacillus ferrooxidans (isolated from arsenopyrite and adapted on sewage sludge) utilized ferrous iron as an energy source in the presence of chloride ions (FeCl₂) as efficiently as ferrous sulphate. No toxic effects of oxalic acid onT. ferrooxidans were observed at the prevailing concentration.     

Photostability and Interaction of Ascorbic Acid in Cream Formulations

The kinetics of photolysis of ascorbic acid in cream formulations on UV irradiation has been studied using a specific spectrophotometric method with a reproducibility of ±5%. The apparent first-order rate constants (k _obs) for the photolysis of ascorbic acid in creams have been determined. The photoproducts formed in the cream formulations include dehydroascorbic acid and 2,3-diketogulonic acid. The photolysis of ascorbic acid appears to be affected by the concentration of active ingredient, pH, and viscosity of the medium and formulation characteristics. The study indicates that the ionized state and redox potentials of ascorbic acid are important factors in the photostability of the vitamin in cream formulations. The viscosity of the humectant present in the creams appears to influence the photostability of ascorbic acid. The results show that the physical stability of the creams is an important factor in the stabilization of the vitamin. In the cream formulations stored in the dark, ascorbic acid undergoes aerobic oxidation and the degradation is affected by similar factors as indicated in the photolysis reactions. The rate of oxidative degradation in the dark is about seventy times slower than that observed in the presence of light.     

Protective effect of seminal plasma proteins on the degradation of ascorbic acid

The objectives of this study were to determine ascorbic acid stability and its effect on antiproteinase activity of seminal plasma in the presence of an oxidant. Effect of seminal plasma, and additives: glutathione, albumin, hydrogen peroxide and Tris buffer, on ascorbic acid degradation was investigated by UV absorbance. Antiproteinase against trypsin amidase activity was measured spectrophotometrically using N-benzoyl-DL-arginine-p-nitroanilide (BAPNA) as substrate. Ascorbic acid was destroyed much more rapidly with the addition of hydrogen peroxide than in Tris buffer at pH 8.2 alone. Seminal plasma protected ascorbic acid more efficiently than glutathione and albumin alone. The protective effect of seminal plasma on ascorbic acid degradation may closely relate to the function of ascorbic acid in reproductive system of scurvy-prone animals including teleost fish. Within the range of 1–8 mM concentrations, ascorbic acid had a pro-oxidant action on seminal plasma antiproteinase activityin vitro when they were incubated with hydrogen peroxide.Abbreviations AA Ascorbic acid - BAPNA N-benzoyl-DL-arginine-p-nitroanilide - DMSO dimethyl sulfoxide - GSH glutathione - H₂O₂ hydrogen peroxide     

抗坏血酸增强氯高铁血红素诱导的溶血

研究抗坏血酸对氯高铁血红素所诱导的红细胞溶血的影响.红细胞溶血采用在540 nm处测定 上清液血红蛋白吸光度的方法;红细胞巴比妥酸反应产物 (TBARS)测定采用Stocks 等建立的方法;高铁血红蛋白的测定采用Sezebeni等报道的方法.结果表明：抗坏血酸显著增强氯高铁血红素所诱导的溶血.尽管氯高铁血红素本身并不影响红细胞TBARS和高铁血红蛋白的水平,但是,氯高铁血红素和抗坏血酸一起诱导红细胞TBARS和高铁血红蛋白含量的增加;过氧化氢酶显著地抑制抗坏血酸增强氯高铁血红素诱导红细胞的溶血、TBARS和高铁血红蛋白的生成;氢氧自由基淬灭剂显著地抑制抗坏血酸增强氯高铁血红素诱导红细胞溶血.由上述可得到如下 结论：抗坏血酸增加氯高铁血红素诱导的红细胞氧化压力与H₂O₂有关;氢氧自由基可能是抗坏血酸增强氯高铁血红素诱导红细胞溶血的原因;抗坏血酸在氯高铁血红素存在时,可以作为一个亲氧化剂而非一个抗氧化剂.     

An investigation into the role of hydroxyl radical in xanthine oxidase-dependent lipid peroxidation

A model lipid peroxidation system dependent upon the hydroxyl radical, generated by Fenton's reagent, was compared to another model system dependent upon the enzymatic generation of superoxide by xanthine oxidase. Peroxidation was studied in detergent-dispersed linoleic acid and in phospholipid liposomes. Hydroxyl radical generation by Fenton's reagent (FeCl₂ + H₂O₂) in the presence of phospholipid liposomes resulted in lipid peroxidation as evidenced by malondialdehyde and lipid hydroperoxide formation. Catalase, mannitol, and Tris-Cl were capable of inhibiting activity. The addition of EDTA resulted in complete inhibition of activity when the concentration of EDTA exceeded the concentration of Fe²⁺. The addition of ADP resulted in slight inhibition of activity, however, the activity was less sensitive to inhibition by mannitol. At an ADP to Fe²⁺ molar ratio of 10 to 1, 10 mm mannitol caused 25% inhibition of activity. Lipid peroxidation dependent on the enzymatic generation of superoxide by xanthine oxidase was studied in liposomes and in detergent-dispersed linoleate. No activity was observed in the absence of added iron. Activity and the apparent mechanism of initiation was dependent upon iron chelation. The addition of EDTA-chelated iron to the detergent-dispersed linoleate system resulted in lipid peroxidation as evidenced by diene conjugation. This activity was inhibited by catalase and hydroxyl radical trapping agents. In contrast, no activity was observed with phospholipid liposomes when iron was chelated with EDTA. The peroxidation of liposomes required ADP-chelated iron and activity was stimulated upon the addition of EDTA-chelated iron. The peroxidation of detergent-dispersed linoleate was also enhanced by ADP-chelated iron. Again, this peroxidation in the presence of ADP-chelated iron was not sensitive to catalase or hydroxyl radical trapping agents. It is proposed that initiation of superoxide-dependent lipid peroxidation in the presence of EDTA-chelated iron occurs via the hydroxyl radical. However, in the presence of ADP-chelated iron, the participation of the free hydroxyl radical is minimal.     

Ascorbic Acid Inhibits [3H]sch-23390 Binding to Striatal Dopamine D1 Receptors

Abstract

The present study describes the inhibition of [³H]SCH-23390 binding to striatal dopamine D₁ receptors in the presence of ascorbic acid. Specific [³H]SCH-23390 binding was maximally inhibited by 0.1 mM ascorbic acid. As determined by Scatchard analysis the binding in the presence of 0.01, 0.1, or 10 mM ascorbic acid was consonant with non-competitive inhibition with a 26%, 38%, or 19% decrease, respectively, in the maximal number of binding sites; the affinity of these binding sites was not affected. Inhibition of [³H]SCH-23390 binding by ascorbic acid was reversible; striatal homogenates incubated with 0.1 mM ascorbic acid and sebsequently washed free of ascorbic acid had the same Scatchard parameters as untreated preparations.     

Intracellular Ascorbic Acid Inhibits the Na+-Ca2+ Exchanger in Cultured Rat Astrocytes

Abstract: The effect of ascorbic acid on Ca²⁺ uptake in cultured rat astrocytes was examined in the presence of ouabain and monensin, which are considered to drive the Na⁺-Ca²⁺ exchanger in the reverse mode. Ascorbic acid at 0.1–1 m M inhibited Na⁺-dependent Ca²⁺ uptake significantly but not Na⁺-dependent glutamate uptake in the cells, although the inhibition required pretreatment for more than 30 min. The effect of ascorbic acid on the Ca²⁺ uptake was blocked by simultaneous addition of ascorbate oxidase (10 U/ml). Na⁺-dependent Ca²⁺ uptake was also inhibited by isoascorbate at 1 m M but not by ascorbate 2-sulfate, dehydroascorbate, and sulfhydryl-reducing reagents such as glutathione and 2-mercaptoethanol. The inhibitory effect of ascorbic acid was observed even in the presence of an inhibitor of lipid peroxidation, o -phenanthroline, or a radical scavenger, mannitol, and the degrading enzymes such as catalase and superoxide dismutase. On the other hand, the inhibitory effect was not observed under the Na⁺-free conditions that inhibited the uptake of ascorbic acid in astrocytes. When astrocytes were cultured for 2 weeks in a medium containing ascorbic acid, the content of ascorbic acid in the cells was increased and conversely Na⁺-dependent Ca²⁺ uptake was decreased. These results suggest that an increase in intracellular ascorbic acid results in a decrease of Na⁺-Ca²⁺ exchange activity in cultured astrocytes and the mechanism is not related to lipid peroxidation.     

The role of iron in enhancing anaerobic toluene degradation in sulfate-reducing enrichment cultures

Ferrous iron enhanced the toluene degradation rate of sulfidogenic enrichment cultures inoculated with contaminated subsurface soil from an aviation fuel storage facility near the Patuxent River (Md.). Ferrous iron had an analogous effect on the degradation rate of benzoic acid, a transient metabolite of anaerobic toluene degradation in these cultures, when benzoic acid was used as a sole carbon and energy source. Two hypotheses were proposed to explain iron's effect: (a) Iron may have prevented sulfide toxicity via precipitation of sulfide as FeS, and (b) iron might have been a limiting nutrient required for degradation (i.e., amendments of iron could have compensated for iron removed from solution by precipitation as FeS). To test these hypotheses, substrate degradation rates were compared in the presence of FeSO₄ (a sulfate source that both precipitates sulfide species and precludes iron limitation) versus ZnSO₄ (a sulfate source that precipitates sulfide species but does not preclude iron limitation) versus MgSO₄ (a sulfate source that neither precipitates sulfide nor precludes iron limitation). For both toluene and benzoic acid, FeSO₄ and ZnSO₄ were comparable in their enhancement of substrate degradation rates and were superior to MgSO₄ in that respect. Thus, iron appears to ameliorate sulfide toxicity, not nutritional iron limitation, in these cultures. The observation that ethylenediaminetetraacetic acid, a chelating agent capable of retaining iron in solution in the presence of sulfide, did not stimulate the cultures is consistent with this conclusion. The implications of these results for bioremediation of fuel-contaminated aquifers that contain sulfate-reducing bacteria are discussed. Correspondence to: H.R. Beller.     

Role of Phosphate and Kinetic Characteristics of Complete Iron Release from Native Pig Spleen Ferritin-Fe

The kinetics for complete iron release showing biphasic behavior from pig spleen ferritin-Fe (PSFF) was measured by spectrophotometry. The native core within the PSFF shell consisted of 1682 hydroxide Fe³⁺ and 13 phosphate molecules. Inhibition kinetics for complete iron release was measure by differential spectrophotometry in the presence of phosphate; the process was clearly divided into two phases involving a first-order reaction at an increasing rate of 46.5 Fe³⁺/PSFF/min on the surface of the iron core and a zero-order reaction at a decreasing rate of 6.67 Fe³⁺/PSFF/min inside the core. The kinetic equation [C(PSFF-Fe³⁺)_max – C(PSFF-Fe³⁺) _t ]^1/2 = T _max –T _t gives the transition time between the two rates and represents the complex kinetic characteristics. The rate was directly accelerated twofold by a mixed reducer of dithionite and ascorbic acid. These results suggest that the channel of the PSFF shell may carry out multiple functions for iron metabolism and storage and that the phosphate strongly affects the rate of iron release.     

Arsenic species that cause release of iron from ferritin and generation of activated oxygen

The in vitro effects of four different species of arsenic (arsenate, arsenite, monomethylarsonic acid, and dimethylarsinic acid) in mobilizing iron from horse spleen ferritin under aerobic and anaerobic conditions were investigated. Dimethylarsinic acid (DMA(V)) and dimethylarsinous acid (DMA(III)) significantly released iron from horse spleen ferritin either with or without the presence of ascorbic acid, a strong synergistic agent. Ascorbic acid-mediated iron release was time-dependent as well as both DMA(III) and ferritin concentration-dependent. Iron release from ferritin by DMA(III)) alone or with ascorbic acid was not significantly inhibited by superoxide dismutase (150 or 300 units/ml). However, the iron release was greater under anaerobic conditions (nitrogen gas), which indicates direct chemical reduction of iron from ferritin by DMA(III), with or without ascorbic acid. Both DMA(V) and DMA(III)) released iron from both horse spleen and human liver ferritin. Further, the release of ferritin iron by DMA(III)) with ascorbic acid catalyzed bleomycin-dependent degradation of calf thymus DNA. These results indicate that exogenous methylated arsenic species and endogenous ascorbic acid can cause (a) the release of iron from ferritin, (b) the iron-dependent formation of reactive oxygen species, and (c) DNA damage. This reactive oxygen species pathway could be a mechanism of action of arsenic carcinogenesis in man.     

Evaluation of Insulin and Ascorbic Acid Effects on Expression of Bcl-2 Family Proteins and Caspase-3 Activity in Hippocampus of STZ-Induced Diabetic Rats

Aims Effects of insulin and ascorbic acid on expression of Bcl-2 family proteins and caspase-3 activity in hippocampus of diabetic rats were evaluated in this study. Methods Diabetes was induced in Wistar male rats by streptozotocin (STZ). Six weeks after verification of diabetes, the animals were treated for 2 weeks with insulin or/and ascorbic acid in separate groups. Hippocampi of rats were removed and evaluation of Bcl-2, Bcl-x_L, and Bax proteins expression in frozen hippocampi tissues were done by SDS-PAGE electrophoresis and blotting. The Bcl-2, Bcl-x_L, and Bax proteins bands were visualized after incubation with specific antibodies using enhanced chemiluminescences method. Caspase-3 activity was determined using the caspase-3/CPP32 Fluorometric Assay Kit. Results Diabetic rats showed increase in Bax protein expression and decrease in Bcl-2 and Bcl-x_L proteins expression. The Bax/Bcl-2 and Bax/Bcl-x_L ratios were found higher compared with non-diabetic control group. Treatments with insulin and/or ascorbic acid were resulted in decrease in Bax protein expression and increase in Bcl-2 and Bcl-x_L proteins expression. The Bcl-2/Bax and Bcl-x_L/Bax ratios were found higher in treated groups than untreated diabetic group. Caspase-3 activity level was found higher in diabetic group compared with non-diabetic group. Treatment with insulin and ascorbic acid did downregulated caspase-3 activity. Conclusions Our data provide supportive evidence to demonstrate the antiapoptotic effects of insulin and ascorbic acid on hippocampus of STZ-induced diabetic rats.     

Attachment of Entamoeba histolytica to Glass in a Defined Maintenance Medium: Specific Requirement for Cysteine and Ascorbic Acid*

SYNOPSIS. Cysteine and ascorbic acid were previously shown to be required by Entamoeba histolytica trophozoites for attachment to glass, elongation, and ameboid movement as well as for short-term (12–24 h) survival in a balanced salt solution containing bovine serum albumin and a vitamin solution (Maintenance Medium 1). If the only function of cysteine and ascorbate was to decrease the redox potential, other reducing agents should be effective. However, the requirement for cysteine in the presence of ascorbic acid was highly specific. Equally effective were D- and L-cysteine; however, of many other compounds tested, only thioglycolic acid, ascorbic acid, or L-cystine (in decreasing order) were somewhat active. Under N₂ atmosphere, cysteine and ascorbic acid were still required, although their concentrations could be halved. The ability to attach in the maintenance medium was irreversibly lost after only 5 min of cysteine-ascorbic acid deprivation; however, there was no decrease in viability when the amebae were transferred to growth medium within 30 min. Cysteine thiol groups in the medium were oxidized rapidly regardless of the concentration of ascorbic acid or the presence of amebae; however, ascorbic acid prolonged attachment of amebae.     

Anemia associated with changes in iron and iron-59 utilization in copper deficient rats fed high levels of dietary ascorbic acid and iron

The influence of dietary copper, iron, and ascorbic acid on iron utilization was examined in a 2×2×2 factorial experiment. Male Sprague-Dawley weanling rats were fed copper-deficient (Cu-, 0.42 μg Cu/g) or copper-adequate (Cu+, 5.74 μg Cu/g) diets that contained one of two levels of iron (38 or 191μg Fe/g) and ascorbic acid (0 or 1% of the diet). These eight diets were fed for 20 d, and rats received an oral dose of 4 μCi iron-59 on d 15. Compared to Cu+ rats, the Cu− rats had 27% lower hemoglobin levels with 45, 59, and 65% lower cytochrome c oxidase (CCO) activities in the liver, heart, and bone marrow, respectively (p<0.0001). High dietary iron or ascorbic acid did not alter hemoglobin in Cu+ rats. However, hemoglobin was 23% lower in Cu− rats fed the highest, rather than the lowest levels of iron and ascorbic acid. Liver CCO was decreased (p<0.02) in Cu− rats fed high iron. Among Cu− rats, ascorbic acid did not influence CCO but decreased hemoglobin by 17% (p<0.001), reduced the percentage of absorbed iron-59 in the erythrocytes by 91% (p<0.05) and depressed the percentage apparent absorption of iron (p<0.05). These results suggest that the effects of elevated dietary iron and ascorbic acid on iron utilization are influenced by copper status.     

The gills as an important uptake route for the essential nutrient iron in freshwater rainbow trout Oncorhynchus mykiss

Short-term (3h) acquisition of iron (16 nmol ⁵⁹FeCl₃ l⁻¹) from oxic, alkaline fresh water was assessed in rainbow trout Oncorhynchus mykiss in the presence or absence of a range of iron chelators, all of which had differing binding affinities for ferric iron [100 μmol l⁻¹ of desferrioxamine (DFO), Log₁₀K₁ 32·5; citric acid Log₁₀K₁ 11·9; nitrilotriacetic acid (NTA) Log₁₀K₁ 15·9, CP20 and CP94 (Log₁₀K₁ > 30), as well as humic acid (HA), Log₁₀K₁ 5·04, 5 mg l⁻¹]. In the absence of chelators (control conditions) O. mykiss acquired iron from the water under laboratory lights (wavelength range of the lights 440–650 nm, peak intensity 548–626 nm) via the gill. In these conditions iron uptake onto the gill had a maximum transport capacity (J_max) of 11·2 pmol Fe g⁻¹ h⁻¹ (gill organ mass) and a K_m of 21·3 nmol Fe l⁻¹ h⁻¹. Furthermore, there were two components to iron accumulation into the carcass of these fish, a slow rate of aqueous iron uptake at low concentrations (6–24 nmol Fe l⁻¹), followed by a faster rate of uptake at higher iron concentrations (48–96 nmol Fe l⁻¹), suggesting that the rate-limiting step of iron uptake at low iron concentrations is the apical entry step. O. mykiss also acquired iron in the presence of HA, although the majority of the other chelators prevented iron uptake. Ultraviolet light (354 nm) treatment of Fe-DFO increased iron bioavailability. Results suggest that rainbow trout are able to access either the predicted very low concentrations (picomolar) of ferrous iron present in fresh water or the ferric oxide complexes present in oxic environments. The iron uptake rate measured (0·75 pmol g⁻¹ h⁻¹) would be sufficient to provide a substantial proportion (c. 85%) of the daily iron requirements of growing salmonid fry.     

纳米铁氧化物对Pelotomaculum schinkii培养系丙酸厌氧降解产甲烷的影响

微生物能利用导电材料进行电子传递,提高种间电子传递效率。铁基纳米导电物质可以加速土壤及厌氧消化系统中微生物间的种间电子传递,促进有机废弃物的产甲烷过程。前期获得了厌氧丙酸富集培养系,互营丙酸氧化菌（Pelotomaculum schinkii）在培养系中占优势,本研究考察了10~4 000 mg/L 纳米铁氧化物对丙酸降解产甲烷过程的作用及微生物的影响。结果表明,低浓度的铁基纳米材料对丙酸降解有一定的促进作用,而高浓度会抑制产甲烷：10~1 000 mg/L纳米Fe₃O₄对产甲烷无明显影响,1 500~4 000 mg/L最大产甲烷速率抑制了26%~80%,延滞期增加了174%~222%;10~200 mg/L纳米Fe₂O₃使最大产甲烷速率提高了21%~29%,1 500~4 000 mg/L最大产甲烷速率抑制了48%~58%,延滞期增加了29%~85%。微生物群落解析结果表明,与对照相比,10~1 000 mg/L纳米Fe₂O₃使P. schinkii相对丰度略有增加,而4 000 mg/L纳米₃O₄/Fe₂O₃使P. schinkii的相对丰度下降了70.7%和55.9%,说明高浓度纳米铁氧化物会抑制P. schinkii的活性,导致丙酸降解及产甲烷速率降低。