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PubMed2002

National audit of citrate toxicity in plateletpheresis donors.

UNLABELLED: Citrate toxicity complicating plateletpheresis is not uncommon. However, the scale and severity of the problem have never been formally addressed. In order to answer these questions we undertook a national audit of 13 070-platelet procedures throughout 17 apheresis centres in England over a 3-month period from 1 April to 30 June 2000. A standard form was distributed to each centre to record the symptoms/signs of citrate toxicity which were then graded (grades 1-5) according to their severity. The following variables were studied to determine whether they influenced the frequency and severity of citrate toxicity: 1. The type of manufacturer's cell separator used (Cobe Spectra, Haemonetics, Baxter Amicus and Trima). 2 The type of procedure: single needle, dual needle, single, double or triple dose. 3 The way in which donors were instructed to report symptoms of citrate toxicity. OUTCOME: Plateletpheresis is a relatively safe procedure provided that donors who experience severe reactions receive appropriate treatment. The incidence of severe citrate toxicity (0.03% procedures) is comparable to that of severe faints following whole blood donation, indicating a comparable margin of safety. Donors should be warned of the symptoms of citrate toxicity at their first attendance only. More frequent reminders encourage donors to over-report symptoms of mild citrate toxicity.

Blood Banks↗
PubMed2006

Association of prevalent hypertension with 24-hour urinary excretion of calcium, citrate, and other factors.

BACKGROUND: The relation between hypertension and the urinary excretion of calcium, citrate, and other factors is unclear. It has been proposed that increased urinary calcium excretion is a central feature of essential hypertension. Metabolic acidosis also may be associated with hypertension and decreases urinary citrate levels. METHODS: To compare the urine composition of individuals with and without hypertension, we studied 24-hour urinary excretion of calcium, citrate, oxalate, uric acid, sodium, magnesium, potassium, phosphorus, and creatinine and pH in a subset of participants with and without nephrolithiasis in the Nurses' Health Study I (older women; N = 1,284), Nurses' Health Study II (younger women; N = 952), and the Health Professionals Follow-up Study (men; N = 788). Logistic regression models adjusted for age, weight, dietary intake, and urinary factors. RESULTS: In participants with and without nephrolithiasis, citrate was the only urinary factor consistently related to hypertension. Compared with those in the lowest quartile of urinary citrate excretion, multivariate odds ratios of prevalent hypertension in the highest quartile were 0.37 (95% confidence interval [CI], 0.24 to 0.55; P trend < 0.001) for older women, 0.54 (95% CI, 0.32 to 0.92; P trend = 0.03) for younger women, and 0.27 (95% CI, 0.16 to 0.45; P trend < 0.001) for men. Urinary calcium levels were not related consistently to hypertension. Excluding participants with single 24-hour urine collections and those administered thiazide diuretics or angiotensin-converting enzyme inhibitors did not change the results. CONCLUSION: Lower urinary citrate excretion is associated independently with prevalent hypertension. Factors that regulate urinary citrate excretion may play a role in hypertension.

Adult↗
PubMed2001

Decreased urinary citrate excretion in type 1a glycogen storage disease.

OBJECTIVES: To quantify urinary citrate and calcium excretion and systemic acid-base status in patients with type 1a glycogen storage disease (GSD1a) and to investigate their relationship to renal complications. STUDY DESIGN: Fifteen patients (7 male and 8 female; age range, 3--28 years) were studied during annual evaluations of metabolic control. All were treated with intermittent doses of uncooked cornstarch. Hourly blood sampling and a 24-hour urine collection were obtained while subjects followed their usual home dietary regimen. RESULTS: All but the youngest subject had low levels of citrate excretion (mean 2.4 +/- 1.8 mg/kg/d; 129 +/- 21 mg citrate/g creatinine). Normally, urinary citrate excretion increases with age; however, in patients with GSD1a, a strong inverse exponential relationship was found between age and citrate excretion (r = -0.84, P <.0001). Urinary citrate excretion was unrelated to markers of metabolic control. Hypercalciuria occurred in 9 of 15 patients (mean urinary calcium/creatinine ratio, 0.27 +/- 0.15) and was also inversely correlated with age (r = -0.62, P =.001). CONCLUSIONS: Hypocitraturia that worsens with age occurs in metabolically compensated patients with GSD1a. The combination of low citrate excretion and hypercalciuria appears to be important in the pathogenesis of nephrocalcinosis and nephrolithiasis. Citrate supplementation may be beneficial in preventing or ameliorating nephrocalcinosis and the development of urinary calculi in GSD1a.

Adolescent↗
PubMed2003

Malate and malate-channel antibodies inhibit electrogenic and ATP-dependent citrate transport across the tonoplast of citrus juice cells.

Citrus juice cells accumulate high levels of citric acid in their vacuoles when compared to other organic ions including malate. Uptake of citrate into tonoplast vesicles from Citrus juice cells was investigated in the presence of malate, and after incubation with antibodies raised against the vacuolar malate-specific channel of Kalanchoë diagremontiana leaves. Antibodies against the vacuolar malate channel immunoreacted with a protein of similar size in tonoplast extracts from three Citrus varieties differing in citric acid content. Malate channel antibodies inhibited both delta MicroH(+)-dependent and delta MicroH(+)-independent ATP-dependent citrate transport, indicating common domains in both transport systems and to the malate-specific channel of Kalanchoë diagremontiana leaves. Malate strongly inhibited electrogenic citrate transport, whereas ATP-dependent citrate uptake was less affected. Kinetic analysis of citrate transport in the presence of malate confirmed the existence of two citrate transport mechanisms and indicated that both citrate and malate share a common transport channel across the tonoplast of Citrus juice cells.

Adenosine Triphosphate↗
PubMed2004

Molecular mapping of a gene responsible for Al-activated secretion of citrate in barley.

Aluminium (Al) toxicity is an important limitation to barley (Hordeum vulgare L.) on acid soil. Al-resistant cultivars of barley detoxify Al externally by secreting citrate from the roots. To link the genetics and physiology of Al resistance in barley, genes controlling Al resistance and Al-activated secretion of citrate were mapped. An analysis of Al-induced root growth inhibition from 100 F2 seedlings derived from an Al-resistant cultivar (Murasakimochi) and an Al-sensitive cultivar (Morex) showed that a gene associated with Al resistance is localized on chromosome 4H, tightly linked to microsatellite marker Bmag353. Quantitative trait locus (QTL) analysis from 59 F4 seedlings derived from an F3 plant heterozygous at the region of Al resistance on chromosome 4H showed that a gene responsible for the Al-activated secretion of citrate was also tightly linked to microsatellite marker Bmag353. This QTL explained more than 50% of the phenotypic variation in citrate secretion in this population. These results indicate that the gene controlling Al resistance on barley chromosome 4H is identical to that for Al-activated secretion of citrate and that the secretion of citrate is one of the mechanisms of Al resistance in barley. The identification of the microsatellite marker associated with both Al resistance and citrate secretion provides a valuable tool for marker-assisted selection of Al-resistant lines.

Adaptation, Physiological↗
PubMed1971

Effect of iron on the transport of citrate into the xylem of soybeans and tomatoes.

Iron transport in soybeans (Glycine max [L] Merr.) and tomatoes (Lycopersicum esculentum) is controlled by factors that are altered manyfold as the plant experiences an iron stress (deficiency). Depending on their response to an Fe stress, plants in this study are classed (a) Fe-inefficient or (b) Fe-efficient. The Fe-efficient plants transport more Fe and concomitantly more citrate than the Fe-inefficient plants.An available supply of Fe added to the plant root will facilitate the release of citrate to the stem exudate in both soybeans and tomatoes. Also, when the iron supply is decreased by trapping Fe(2+) at the root, Fe transport decreases with a concomitant decrease of citrate in the stem exudate. Factors other than citrate appear to affect movement of Fe from the external solution into root cells where Fe is chelated with citrate and moves thereafter as Fe citrate. This makes some of the citrate that is transported in the stem exudate dependent on the amount of Fe made available at the root.

Journal Article↗
PubMed1979

Citrate and succinate uptake by potato mitochondria.

The uptake of [(14)C]citrate and [(14)C]succinate was studied in potato mitochondria (Solanum tuberosum var. Russet Burbank) using cellulose pore filtration and was found to occur by the same mechanisms as described for mammalian mitochondria. Potato mitochondria, in the absence of respiration, have a very low capacity for uptake by exchange with endogenous anions, taking up only 2.4 nanomoles citrate and 2.0 nanomoles succinate per milligram protein. Maximum citrate uptake of over 17 nanomoles per milligram protein occurs in the presence of inorganic phosphate, a dicarboxylic acid, and an external energy source (NADH), conditions where net anion accumulation proceeds, mediated by the interlinking of the inorganic phosphate, dicarboxylate, and tricarboxylate carriers. Maximum succinate uptake in the absence of respiratory inhibitors requires only added inorganic phosphate.Compounds which inhibit respiration (antimycin), the exchange carriers (mersalyl and benzylmalonate), or the establishment of the membrane proton motive force (uncouplers) reduce substrate accumulation. A potent inhibitor of the citrate carrier in animal mitochondria, 1,2,3-benzenetricarboxylic acid, does not inhibit citrate uptake in potato mitochondria. Citrate uptake is reduced by concurrent ADP phosphorylation and this reduction is sensitive to oligomycin. The initiation of state 3 after a 3-minute substrate state results in a reduction of the steady-state of citrate uptake by approximately 50%. Accumulation of succinate initially is inhibited by increasing sucrose concentration in the reaction medium from 50 to 400 millimolar.Limited substrate uptake is one of the factors responsible for the often observed depressed initial state 3 respiration rates in many mitochondrial preparations. Since nonlimiting levels of substrate in the matrix cannot be attained by energy-independent exchange, a dependence on respiration for adequate uptake results. Substrate limitation therefore occurs in the matrix for the period of time needed for energy-dependent accumulation of nonlimiting levels.

Journal Article↗
PubMed1987

Transport Properties of the Tomato Fruit Tonoplast : II. Citrate Transport.

Citrate transport across the membrane of tomato fruit tonoplast vesicles was investigated. In the tonoplast vesicles, [(14)C]methylamine uptake was stimulated 10-fold by MgATP and strongly inhibited by NO(3) (-). Under identical experimental conditions, [(14)C]citrate uptake was inhibited by 5 millimolar free Mg(2+), and this inhibition was reversed in the presence of ATP, presumably by ATP chelation of free Mg(2+). No evidence was obtained in support of energy-linked ATP stimulation of citrate uptake. Citrate uptake showed saturation kinetics, and was inhibited by 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid and by other organic acids. The pH-dependence of uptake suggested that citrate(3-) was the transported species. Our results indicate that citrate transport across the tomato fruit tonoplast occurs by facilitated diffusion of citrate(3-). The carrier shares some features in common with anion channels in that it is relatively nonspecific for organic acids and is inhibitable by 4,4'-diisothyocyano-2,2'-stilbenedisulfonic acid.

Journal Article↗
PubMed1995

Enzyme Basis for pH Regulation of Citrate and Pyruvate Metabolism by Leuconostoc oenos.

Citrate and pyruvate metabolism by nongrowing cells of Leuconostoc oenos was investigated. (sup13)C nuclear magnetic resonance (NMR) spectroscopy was used to elucidate the pathway of citrate breakdown and to probe citrate or pyruvate utilization, noninvasively, in living cell suspensions. The utilization of isotopically enriched substrates allowed us to account for the end products derived from the metabolism of endogenous reserves. The effect of environmental parameters, e.g., pH, gas atmosphere, and presence of malate, on the end products of citrate utilization was studied. Approximately 10% of the citrate supplied was converted to aspartate which remained inside the cells. A metabolic shift with pH was observed, with acetoin production being favored at pH 4, whereas lactate and acetate production increased significantly at higher pH values. The information obtained with NMR was complemented with studies on the relevant enzyme activities in the metabolic pathway of citrate breakdown. The intracellular pH of the cells was strongly dependent on the external pH; this result, together with the determination of the pH profile of the enzymic activities, allowed us to establish the basis for pH regulation; lactate dehydrogenase activity was optimal at pH 7, whereas the acetoin-forming enzymes displayed maximal activities below pH 5. Citrate utilization was also monitored in dilute cell suspensions for comparison with NMR experiments performed with dense suspensions.

Journal Article↗
PubMed1998

The citrate transport system of Lactococcus lactis subsp. lactis biovar diacetylactis is induced by acid stress.

Citrate transport in Lactococcus lactis subsp. lactis biovar diacetylactis is catalyzed by citrate permease P (CitP), which is encoded by the plasmidic citP gene. We have shown previously that citP is included in the citQRP operon, which is mainly transcribed from the P1 promoter in L. lactis subsp. lactis biovar diacetylactis. furthermore, transcription of citQRP and citrate transport are not induced by the presence of citrate in the growth medium. In this work, we analyzed the influence of the extracellular pH on the expression of citP. The citrate transport system is induced by natural acidification of the medium during cell growth and by a shift to media buffered at acidic pHs. This inducible response to acid stress takes place at the transcriptional level and seems to be due to increased utilization of the P1 promoter. Increased transcription correlates with increased synthesis of CitP and results in higher citrate transport activity catalyzed by the cells. Finally, this acid stress response seems to provide L. lactis subsp. lactis biovar diacetylactis with a selective advantage resulting from cometabolism of glucose and citrate at low pHs.

Bacterial Proteins↗
PubMed2000

Citrate enhances olfactory receptor responses and triggers oscillatory receptor activity in the channel catfish.

Citrate, a normal constituent of cellular metabolism, in a binary mixture with an amino acid enhanced asynchronous olfactory receptor responses in the channel catfish, Ictalurus punctatus. In addition, high concentrations of either citrate (> or =3 mM) alone or an amino acid (> or =0.1 mM) in a binary mixture with citrate (> or =1 mM) triggered synchronized voltage oscillations of olfactory receptor neurons (ORNs) known as "peripheral waves" (PWs). Binary mixtures containing lower concentrations of an amino acid also triggered PW activity if the concentration of citrate in the mixture was increased. Both the enhancement of asynchronous activity and the generation of PW activity were the result of citrate chelating calcium, which lowers the surface potential of ORNs making them hyperexcitable. These effects of citrate are replicated by EGTA. Inactivation of the chelating ability of citrate and EGTA with 1 mM calcium chloride, barium chloride, or strontium chloride abolished both the enhancement of asynchronous olfactory responses and PW activity, while not affecting olfactory receptor responses to the amino acids alone.

Action Potentials↗
PubMed2005

Citrate reverses cyclosporin A-induced metabolic acidosis and bone resorption in rats.

BACKGROUND: Cyclosporine A (CsA) causes distal renal tubular acidosis (RTA) and osteoporosis. We have recently reported that the reduction of nitric oxide (NO) exacerbates this condition. Distal RTA may deplete bone mineral due to the chronic buffering of acid in the blood. The interaction of CsA and NO in causing metabolic acidosis and bone demineralization has not been studied previously. Nor has the salubrious effect of citrate therapy. PURPOSE: To examine the effect of systemic pH correction by citrate on renal electrolyte (Na, K, Cl, NH3, HCO3) excretion following acute water loading in CsA-treated and NO-reduced rats. We further evaluated femoral bone density and bone demineralization activity after the same treatments. METHODS: Rats received CsA, L-arginine (L-Arg), or nitro-L-arginine-methyl ester (L-NAME), or a combination of CsA+L-NAME plus or minus citrate. Urine and blood electrolytes were examined, as well as the urine excretion of deoxypyridinoline and the bone density of both femurs. RESULTS: CsA and L-NAME reduced urine pH and the serum HCO3- concentration, and increased serum K+ and Cl- concentrations. The combination of CsA with L-NAME caused more severe deficits in the serum HCO3- concentration and elevations in serum K+ and Cl- concentrations than either drug alone. Both CsA and L-NAME reduced urinary nitrate excretion, which was reversed by co-administration of L-Arg. Co-administration of citrate or L-Arg improved the CsA- and L-NAME-induced acidosis and hyperkalemia. Bone resorption and density of the femurs were decreased by CsA and L-NAME and were additive for both drugs. Co-administration of citrate or L-Arg restored both bone resorption and density to normal levels. CONCLUSION: CsA induces a hyperchloremic metabolic acidosis with hyperkalemia and a reduction in NO. The ensuing systemic acidosis causes bone resorption and demineralization. These effects were corrected by co-treatment with citrate. Citrate, at least in part, directly reduces the protonation of bone in animals treated with CsA and is recommended as a potential adjunct drug to prevent bone demineralization in patients chronically receiving CsA.

Acidosis↗
PubMed1997

Rapid loss of fentanyl citrate admixed with fluorouracil in polyvinyl chloride containers.

OBJECTIVE: To study the physical compatibility and chemical stability of fluorouracil 1 and 16 mg/mL with fentanyl citrate 12.5 micrograms/mL in dextrose 5% and in sodium chloride 0.9% injection. DESIGN: Test solutions of the drugs in dextrose 5% injection and in sodium chloride 0.9% injection were prepared in triplicate and stored at -20, 4, 23, and 32 degrees C. Samples were removed immediately and at various times over 7 days and stored at -70 degrees C until analyzed. Physical compatibility was assessed visually and by measuring turbidity with a color-correcting turbidimeter; particle content was measured with a light-obscuration particle sizer and counter. Chemical stability was determined by measuring the concentration of each drug in the test solutions in duplicate with stability-indicating HPLC. RESULTS: Fentanyl citrate was rapidly lost when admixed with fluorouracil in polyvinyl chloride (PVC) containers, losing about 25% in the first 15 minutes and about 50% in the first hour. The loss of fentanyl citrate was so rapid that accurate time zero determinations were not possible. The extent of fentanyl loss increased with time and occurred more rapidly at the higher temperatures (i.e., 23, 32 degrees C). Losses of 70% or more occurred in all samples within 24 hours. Fentanyl underwent rapid sorption to the containers at the high pH (9.0-9.5) of the fluorouracil admixtures. Adjusting the pH of a fentanyl citrate solution (containing no fluorouracil) in PVC containers to pH 9 with sodium hydroxide also resulted in rapid sorption loss. Fentanyl citrate sorption did not occur when admixtures were prepared in polyethylene containers. Fluorouracil remained stable for at least 7 days at all temperatures. There were no visual or subvisual changes in turbidity or particle content in any of the test solutions at any time. CONCLUSIONS: When admixed with fluorouracil 1 and 16 mg/mL in dextrose 5% injection and sodium chloride 0.9% injection, fentanyl citrate 12.5 micrograms/mL underwent rapid and extensive loss due to sorption to the PVC containers, making the combination unacceptable within minutes of mixing. The sorption results from the alkaline pH of the admixture and, presumably, could occur from the admixture of fentanyl citrate with any sufficiently alkaline drug.

Analgesics, Opioid↗
PubMed2005

Measurement of citrate in urine using liquid chromatography tandem mass spectrometry: comparison with an enzymatic method.

BACKGROUND: Measurement of urine citrate is used to assess the risk of further urinary stone formation and to assess the benefit of treatment in affected individuals. We wanted to develop a simple and rapid liquid chromatography tandem mass spectrometry (LC-MS/MS) method for the analysis of urinary citrate and to compare it with our current enzymatic assay. METHODS: For the LC-MS/MS assay, samples were prepared in a deep-well block by adding 10 microL of urine and 20 microL of internal standard to 400 microL of water. After mixing, 3 microL of the diluted sample was injected into the LC-MS/MS system. An LC system was used to isocratically elute a C18 column (50 x 2.1 mm) with 0.4 mL/min water containing 2 mmol/L ammonium acetate and 0.1% (v/v) formic acid. A step gradient of 100% methanol containing 2 mmol/L ammonium acetate and 0.1% (v/v) formic acid was used to wash the column. The retention times were 1.4 min for citrate and 1.4 min for d4-citrate. Cycle time was 4.0 min, injection to injection. The analytes were monitored using a tandem mass spectrometer operated in multiple reaction monitoring mode using the following transitions, citrate m/z 191.0>111.0 and d4-citrate m/z 195.0>113.0. RESULTS: Within and between-batch coefficients of variation were <3% over the range 480-3800 micromol/L. The lower limit of quantification was 24.0 micromol/L. Regression analysis showed LC-MS/MS = 0.8781 (enzymatic assay) + 102.5, r = 0.964, n = 73. CONCLUSIONS: We have developed a simple LC-MS/MS method for urinary citrate measurement that shows acceptable performance.

Chromatography, High Pressure Liquid↗
PubMed1998

Ranitidine bismuth citrate in the treatment of Helicobacter pylori infection and duodenal ulcer.

OBJECTIVE: To review the clinical pharmacology of ranitidine bismuth citrate in the treatment of Helicobacter pylori (HP) infection and duodenal ulcer. DATA SOURCES: A MEDLINE search of the English-language literature from 1992 to January 1997 was conducting using the key terms Tritec, ranitidine, and bismuth. References of articles pertaining to treatment of duodenal ulcer or HP were extensively searched for relevant sources. DATA EXTRACTION: All articles pertaining to ranitidine bismuth citrate were considered for inclusion, with emphasis placed on randomized, double-blind trials. Priority was placed on data pertaining to regimens that are currently approved by the Food and Drug Administration for the treatment of duodenal ulcer in conjunction with HP. DATA SYNTHESIS: Each tablet of ranitidine bismuth citrate 400 mg contains 162 mg of ranitidine base, 128 mg of trivalent bismuth, and 110 mg of citrate. It uses the acid-suppressive actions of ranitidine and the antimicrobial and mucosal protective effects of bismuth to eradicate HP. Ranitidine bismuth citrate in conjunction with clarithromycin represents one of four treatment regimens currently approved in the US for duodenal ulcer associated with HP infection. In four double-blind, randomized trials, this agent has achieved HP eradication rates of 73-94% and duodenal ulcer healing rates of 73-89%. It is given twice daily for 28 days, and is associated with very low rates of adverse effects. CONCLUSIONS: Relative to some therapeutic alternatives, ranitidine bismuth citrate plus clarithromycin may be simpler to take and have less adverse effects, but may be more expensive. Compared with omeprazole plus clarithromycin, it is less expensive, may have lower ulcer healing rates, but may be more effective in eradicating HP. The role of ranitidine bismuth citrate will continue to evolve as more patients are treated, and other regimens continue to be tested for duodenal ulcer healing and HP eradication.

Anti-Ulcer Agents↗
PubMed1997

Direct effect of inorganic mercury on citrate uptake by isolated rat renal brush border membrane vesicles.

Occupational exposure to mercury has long been associated with renal proximal injury and an increased incidence of proteinuria, as has such exposure to cadmium. Renal citrate excretion is very important with respect to acid-base balance since the metabolism of citrate generates three bicarbonate ions. In this study, we exposed isolated rat renal brush border membrane vesicles (BBMV) to mercury (Hg2+) and examined their citrate uptake characteristics. BBMV were prepared by the divalent cation precipitation method. Citrate uptake was measured by the Millipore rapid membrane filtration method. The preincubation of BBMV with 0.5 and 2 mM HgCl2 for 1 min significantly inhibited citrate uptake compared with that of BBMV without Hg preincubation. The analysis of the time course of citrate uptake during a 30-min preincubation of BBMV with 0.1 mM Hg2+ also revealed a significant reduction in the uptake compared with that of the control BBMV without preincubation. These findings indicate that the preincubation of BBMV with mercury results in a time- and concentration-dependent inhibition of citrate uptake.

Animals↗
PubMed1976

Studies on the mode of action of clomiphene citrate.

In order to further investigate the mode of action of clomiphene citrate, 5 oophorectomized women in the age range 28 to 41 years were followed with weekly determinations of serum FSH and LH for 20 weeks after the operation. They received no treatment during the first 4 weeks but during the next 16 weeks they were given estradiol 2 mg X 2 daily orally, and from the 12th to the 16th week in addition clomiphene citrate 50 mgX2 daily. The high level of FSH after the oophorectomy decreased gradually during the treatment with estradiol alone, but this effect was partly neutralized by clomiphene citrate, as we observed a significant increase in FSH within 1 week of initiating treatment with clomiphene citrate. On the other hand, we did not find any significant changes in FSH within 4 weeks after treatment with clomiphene citrate was discontinued. The high level of LH after oophorectomy did not show any significant changes during the whole treatment period. It is concluded that clomiphene citrate primarily stimulated FSH secretion, most probably by a competition with estradiol for the receptor sites in the hypothalamus or the pituitary. In addition, it is concluded that clomiphene citrate has a prolonged effect, probably because of a tight binding to the receptor sites.

Administration, Oral↗
PubMed1999

Role of Fe(III) in Fe(II)citrate-mediated peroxidation of mitochondrial membrane lipids.

In this report we study the effect of Fe(III) on lipid peroxidation induced by Fe(II)citrate in mitochondrial membranes, as assessed by the production of thiobarbituric acid-reactive substances and antimycin A-insensitive oxygen uptake. The presence of Fe(III) stimulates initiation of lipid peroxidation when low citrate:Fe(II) ratios are used (< or = 4:1). For a citrate:total iron ratio of 1:1 the maximal stimulation of lipid peroxidation by Fe(III) was observed when the Fe(II):Fe(III) ratio was in the range of 1:1 to 1:2. The lag phase that accompanies oxygen uptake was greatly diminished by increasing concentrations of Fe(III) when the citrate:total iron ratio was 1:1, but not when this ratio was higher. It is concluded that the increase of lipid peroxidation by Fe(III) is observed only when low citrate:Fe(II) ratios were used. Similar results were obtained using ATP as a ligand of iron. Monitoring the rate of spontaneous Fe(II) oxidation by measuring oxygen uptake in buffered medium, in the absence of mitochondria, Fe(III)-stimulated oxygen consumption was observed only when a low citrate:Fe(II) ratio was used. This result suggests that Fe(III) may facilitate the initiation and/or propagation of lipid peroxidation by increasing the rate of Fe(II)citrate-generated reactive oxygen species.

Animals↗