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At least 19 recordsLinked to original sources
PubMed2001

Final report on the safety assessment of PEG-25 propylene glycol stearate, PEG-75 propylene glycol stearate, PEG-120 propylene glycol stearate, PEG-10 propylene glycol, PEG-8 propylene glycol cocoate, and PEG-55 propylene glycol oleate.

The ingredients considered in this safety assessment are polyethylene glycol ethers of either propylene glycol itself, propylene glycol stearate, propylene glycol oleate, or propylene glycol cocoate. They function in cosmetic formulations as surfactant--cleansing agents; surfactant-solubilizing agents; surfactant--emulsifying agents; skin conditioning agents--humectant; skin-conditioning agents--emollient; and solvents. Those in current use are used in only a small number of cosmetic formulations. Some are not currently used. Polyethylene Glycol (PEG) Propylene Glycol Cocoates and PEG Propylene Glycol Oleates are produced by the esterification of polyoxyalkyl alcohols with lauric acid and oleic acid, respectively. Although there is no information available on the method of manufacture of the other polymers, information was available describing impurities, including ethylene oxide (maximum 1 ppm), 1,4-dioxane (maximum 5 ppm), polycyclic aromatic compounds (maximum 1 ppm), and heavy metals-lead, iron, cobalt, nickel, cadmium, and arsenic included (maximum 10 ppm combined). In an acute oral toxicity study, PEG-25 Propylene Glycol Stearate was not toxic. An antiperspirant product containing 2.0% PEG-25 Propylene Glycol Stearate was nonirritating to mildly irritating to the eyes of rabbits. This product was also practically nonirritating to the skin of rabbits in single-insult occlusive patch tests. In a guinea pig sensitization test, PEG-25 Propylene Glycol Stearate was classified as nonallergenic at challenge concentrations of 25% and 50% in petrolatum. PEG-25 Propylene Glycol Stearate and PEG-55 Propylene Glycol Oleate were negative in clinical patch tests. Based on the available data, it was concluded that these ingredients are safe as used (concentrations no greater than 10%) in cosmetic formulations. Based on evidence of sensitization and nephrotoxicity in burn patients treated with a PEG-based antimicrobial preparation, the ingredients included in this review should not be used on damaged skin.

Animals↗
PubMed1993

Simultaneous determination of ethylene glycol, propylene glycol, 1,3-butylene glycol and 2,3-butylene glycol in human serum and urine by wide-bore column gas chromatography.

A method has been developed for the separation and measurement of ethylene glycol and three other glycols (propylene glycol, 1,3-butylene glycol and 2,3-butylene glycol) in biological samples by wide-bore column gas chromatography with a flame ionization detector. The method used 1,3-propylene glycol (1,3-propanediol) as an internal standard. The method was linear at least from 2 to 1000 micrograms/ml, with a detection limit of 1 microgram/ml. Analytical recoveries were 89-98% for the different concentrations. Precision studies showed coefficients of variation of 1.5-7.7% for the different concentrations. The assay was applied to the analysis of biological samples from two patients who had ingested ethylene glycol and/or other glycols in a suicide attempt.

Adult↗
PubMed1987

[Carcinogenic activity of ethylene oxide and its reaction products 2-chloroethanol, 2-bromoethanol, ethylene glycol and diethylene glycol. III. Research on ethylene glycol and diethylene glycol for carcinogenic effects].

Ethylene glycol and diethylene glycol were each administered once weekly subcutaneously to groups of 100 female NMRI mice at 3 dosages (30; 10 und 3 mg single dose per mouse). Tricaprylin was used as solvent. The mean total dosage per mouse was 2110.5; 707.0 and 196.2 mg for ethylene glycol and 2029.8; 671.7 and 213.3 mg for diethylene glycol. Neither ethylene glycol nor diethylene glycol induced tumors at the injection site or away from the point of administration.

Animals↗
PubMed1991

Antibacterial and antifungal properties of propylene glycol, hexylene glycol, and 1,3-butylene glycol in vitro.

The antimicrobial properties of three glycols, - propylene glycol, hexylene glycol, and 1,3-butylene glycol - against Candida albicans, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes A, Streptococcus mitis, and E. coli were studied in vitro. Within 20 h, 10% and 30% hexylene glycol in fresh tryptic soy broth were able to kill all the micro-organisms listed above. Five percent hexylene glycol showed some antimicrobial properties but the 1% agent had no effect. Thirty percent 1,3-butylene glycol and 30% propylene glycol were approximately as effective as 10% HG. The results speak in favour of using hexylene glycol in cosmetic and dermatological vehicles instead of propylene glycol and 1,3-butylene glycol.

Anti-Bacterial Agents↗
PubMed2003

Effect of vitamin D3 on the conversion of ethylene glycol to glycolate and oxalate in ethylene glycol-fed rats.

Hypercalciuria and hyperoxaluria are important risk factors in the pathogenesis of kidney stones. Urinary glycolate has also been reported to be elevated in patients with renal stones. 1,25-Dihydroxyvitamin D(3), the active metabolite of vitamin D, has been reported to induce hyperoxaluria after either oral or intravenous administration. 1-alpha-D(3), a synthetic derivative of vitamin D, together with ethylene glycol, has been reported to induce renal stones in experimental rats. We have examined the effect of 1-alpha-vitamin D(3) on urinary oxalate and glycolate excretion. Our results indicate that 1-alpha-D(3), together with ethylene glycol, caused a significant increase in urinary glycolate, without a parallel rise in urinary oxalate excretion, in ethylene glycol-fed rats. This increase in urinary glycolate was due to the synergistic effect of both drugs.

Administration, Oral↗
PubMed1975

[Heat resistance of "Bacillus subtilis" and "Bacillus stearothermophilus" spores in ethylene glycol, propylene glycol and butylene glycol solutions. Criticism of the use of thermodynamic parameters (author's transl)].

Increasing concentrations of ethylene glycol (EG), 1,2-propylene glycol (PG) or 2,3-butylene glycol (BG) lower the heat resistance of B. subtilis SJ2 and B. stearothermophilus 1518 spores, and there is a linear relationship between logarithm of decimal reduction time (D) and glycol concentration. D120 degreesc values of B. subtilis spores in 0.02M, pH 7.0 phosphate buffer containing 20 per cent (w/w) EG, PG and BG are respectively 1, 0.7 and 1.1 min compared to 1.5 min in buffer alone. Corresponding values for B. stearothermophilus spores are 2, 2.4 and 3 min compared to 3.2 min. The type of glycol has little effect upon temperature coefficient z for destruction of the B. subtilis spores (average 6.9 degrees C). On the contrary, in the case of B. stearothermophilus, z increases when the number of carbons increases in the glycol molecule (from 7 to 15 degrees). The thermodynamic parameters which characterize the activation of the spore destruction reaction cannot lead to a general conclusion about a possible mechanism of destruction in the presence of chemical compounds belonging to an homologous series: the two behave diversely, and there is no "isokinetic temperature".

Bacillus subtilis↗
PubMed1990

Taste responses of dogs to ethylene glycol, propylene glycol, and ethylene glycol-based antifreeze.

Although it is widely believed that ethylene glycol-based antifreeze (AF) is an attractive tastant to dogs and other animals, empirical data on this point are not available. In experiment 1, we examined the propensity of 178 adult mixed-breed dogs to approach, sniff, and lick a concentration of AF commonly used in automotive cooling systems (50%). Despite the fact that most of the dogs approached and sniffed the AF in these 5-minute tests, only 9% initiated lick responses and most of these were brief and not followed by additional licking. In experiment 2, the lick responses of five gastric-cannulated dogs to aqueous solutions of 20% sucrose, 50% ethylene glycol, 50% propylene glycol, water, and 50% AF were examined in 14-minute tests before and after periods of food and water deprivation. Under the latter conditions, 2 of the 5 dogs drank amounts of ethylene glycol that would have been lethal to uncannulated dogs. None of the five dogs drank potentially lethal amounts of AF. The preference order for these tastants was sucrose greater than water greater than ethylene glycol greater than AF = propylene glycol. Although these findings question the general belief that AF is highly palatable to most dogs, they do imply that large individual differences in responsiveness exist and that AF ingestion is likely influenced by motivational state. Furthermore, they suggest the possibility that unpleasant-tasting additives could be successfully developed to eliminate the ingestion of AF, because the initial attractiveness of AF is relatively low. Such additives would have to be stable in vehicular cooling systems and not adversely affect the functional aspects of AF performance.

Animals↗
PubMed2003

Antitumor properties of irinotecan-containing nanoparticles prepared using poly(DL-lactic acid) and poly(ethylene glycol)-block-poly(propylene glycol)-block-poly(ethylene glycol).

Irinotecan-containing nanoparticles (NP) were prepared by coprecipitation with addition of water to acetone solution of poly(DL-lactic acid), poly(ethylene glycol)-block-poly(propylene glycol)-block-poly(ethylene glycol) and irinotecan, and subsequent evaporation of organic solvent. NP were purified by gel filtration and used for experiments after condensation by evaporation. The obtained NP showed the drug content of 4.5% (w/w) and the mean particle diameter of 118 nm with the particle diameter distribution between 80-210 nm. When the antitumor effect was examined at a repeated dose of 20 mg irinotecan eq/kg for 3 d (3 x 20 mg/kg) using mice bearing Sarcoma 180 subcutaneously, only NP suppressed tumor growth significantly. After i.v. injection in rats, NP maintained irinotecan plasma concentration longer than CPT-11 aqueous solution. The present nanoparticle formation is suggested as a possibly useful dosage form of irinotecan against solid tumor.

Animals↗
PubMed2001

Ethylene glycol toxicity: the role of serum glycolic acid in hemodialysis.

OBJECTIVE: To correlate serum glycolic acid levels with clinical severity and outcome in ethylene glycol poisoning and to determine if glycolic acid levels are predictive of renal failure and the need for hemodialysis. METHODS: We measured serum ethylene glycol and glycolic acid levels by gas chromatography/mass spectrometry for 41 admissions (39 patients) for ethylene glycol ingestion and performed retrospective chart reviews. RESULTS: Eight patients died, all of whom developed acute renal failure. Of the survivors, 15 also developed acute renal failure, whereas 18 did not. Of those with normal renal function, 8 had glycolic acid levels below detection limits (< 0.13 mmol/L) despite ethylene glycol levels as high as 710 mg/dL; 7 of these patients coingested ethanol. Pertinent initial laboratory data for each group are as follows (mean; range): Deceased: pH 6.99 (6.82-7.22); bicarbonate, 4.8 mmol/L (2-9); anion gap, 28.6 mmol/L (24-40); glycolic acid, 23.5 mmol/L (13.8-38.0); ethylene glycol, 136.5 mg/dL (6-272). Survived/acute renal failure: pH 7.07 (6.75-7.32); bicarbonate, 5.6 mmol/L (1-12); anion gap, 28.7 mmol/L (18-41); glycolic acid, 20.2 mmol/L (10.0-30.0); ethylene glycol, 238.8 mg/dL (12-810). No acute renal failure with glycolic acid > 1.0 mmol/L: pH 7.29 (7.12-7.46); bicarbonate, 14.7 mmol/L (4-23); anion gap, 16.5 mmol/L (10-26); glycolic acid, 6.8 mmol/L (2.6-17.0); ethylene glycol, 269.1 mg/dL (6-675). No acute renal failure with glycolic acid < 1.0 mmol/L: pH 7.41 (7.38-7.47); bicarbonate, 23.4 mmol/L (17-25); anion gap, 11.8 mmol/L (8-18); glycolic acid, 0.1 mmol/L (0-0.66); ethylene glycol, 211 mg/dL (8-710). The mean time postingestion to admission generally correlated with severity as follows: deceased, > or = 10.4 h; survived/acute renal failure, > or = 9.9 h; no acute renal failure with glycolic acid > 1.0 mmol/L, > or = 6.2 h; no acute renal failure with glycolic acid < 1.0 mmol/L, > or = 3.7 h. Hematuria was more prevalent than oxaluria (86% and 41%, respectively), but neither was individually predictive of acute renal failure. Good correlations were found between glycolic acid levels and anion gap (r2 = 0.7724), pH (r2 = 0.7921), and bicarbonate (r2 = 0.6579); poor correlations (r2 < 0.0023) occurred between ethylene glycol levels and glycolic acid, pH, anion gap, and bicarbonate. Measured ethylene glycol values were highly correlated with ethylene glycol values calculated from the osmolal gap (r2 = 0.9339), but the latter overestimates the true value by about 7%, on average. An initial glycolic acid level > or = 10 mmol/L predicts acute renal failure with a sensitivity of 100%, a specificity of 94.4%, and an efficiency of 97.6%. Ethylene glycol levels are not predictive of acute renal failure or central nervous system manifestations of toxicity. If only ethylene glycol values are available (measured or calculated), an initial anion gap > 20 mmol/L is 95.6% sensitive and 94.4% specific for acute renal failure when ethylene glycol is present. Likewise, initial pH < 7.30 is 100% sensitive and 88.5% specific for acute renal failure. CONCLUSION: We propose glycolic acid > 8 mmol/L as a criterion for the initiation of hemodialysis in ethylene glycol ingestion. Patients with glycolic acid < 8 mmol/L probably do not need dialysis, regardless of the ethylene glycol concentration, when metabolism of ethylene glycol is therapeutically inhibited. In the absence of glycolic acid values, an anion gap > 20 mmol/L or pH < 7.30 predicts acute renal failure.

Bicarbonates↗
PubMed1998

Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. META Study Group.

OBJECTIVE: Toxic manifestations following ethylene glycol exposure are due to accumulation of metabolites, particularly glycolate. We characterized glycolate elimination kinetics and dialysis properties in a series of ethylene glycol poisonings. METHODS: Patients who ingested ethylene glycol and received fomepizole (4-methylpyrazole; 4-MP) +/- hemodialysis were prospectively evaluated. Serial blood samples for ethylene glycol, glycolate, pH, and bicarbonate were drawn to determine glycolate elimination rate, t1/2, and correlations between initial glycolate and initial markers of acidosis. Dialyzer inlet and outlet samples were obtained to measure hemodialysis glycolate clearance. Plasma ethylene glycol and glycolate were determined by gas chromatography. RESULTS: Ten patients, mean age 49 years (range 28-73 years), presented a mean of 10.5 hours (range 3.5-21.5 hours) after ethylene glycol ingestion. Mean initial ethylene glycol was 18.5 mmol/L (range 0.8-62.2 mmol/L) (115 mg/dL; range 5-386 mg/dL) and glycolate was 17.0 mmol/L (range 10.0-23.7 mmol/L). Nine of 10 underwent hemodialysis. Nonhemodialysis (n = 4) elimination rate was 1.08 +/- 0.67 mmol/L/h (mean +/- SD) and t1/2 was 626 +/- 474 minutes. Elimination t1/2 during hemodialysis (n = 8) was 155 +/- 42 minutes. Hemodialysis clearance (n = 5) was 170 +/- 23 mL/min with flow rates 250-400 mL/min. Pearson correlation coefficients were: anion gap vs glycolate r2 = 0.65 (p = 0.005), bicarbonate vs glycolate r2 = 0.10 (NS) and pH vs glycolate r2 = 0.06 (NS). CONCLUSION: Glycolate has a slow elimination rate and long half-life. Hemodialysis effectively clears glycolate. An increased anion gap correlates with the presence of glycolate. Hemodialysis is projected as useful for ethylene glycol-poisoned patients with anion gap acidosis and low ethylene glycol blood levels.

Adult↗
PubMed2002

Clinical toxicologic implications of ethylene glycol and glycolic acid poisoning.

Metabolic pathways have been elucidated for various chemical and solvent exposures in humans. Clinical laboratory analyses in most chemical and solvent exposures are directed toward identification and quantitation of unchanged substance in serum or whole blood. For example, most laboratories routinely screen for unchanged ethylene glycol in suspected poisonings and quantitate ethylene glycol in positive cases even though toxicity from ethylene glycol exposure (including central nervous system depression, acute renal failure, and elevated anion gap metabolic acidosis) is primarily caused by one metabolite-glycolic acid. One objective of this manuscript is to describe the authors' clinical experience with glycolic acid analysis in ethylene glycol human poisonings. Recommended clinical laboratory tests for small hospitals and toxicology reference laboratories are presented to rule out or confirm ethylene glycol exposure. Another concern with laboratory support in ethylene glycol poisoning is correct identification of ethylene glycol because analysis of this substance is often problematic. In one case laboratories incorrectly identified an organic acid from an inherited metabolic disease as ethylene glycol, and in another case the intentional ethylene glycol poisoning of an infant was determined to be the results of an endogenous organic acid. The most robust analytical methods for determining ethylene glycol and glycolic acid are chromatographic methods. Ideally, screening methods for ethylene glycol should be confirmed by another method based on a different principle of analysis or include simultaneous metabolite analysis (glycolic acid). In centers where several ethylene glycol cases present annually, toxicology laboratories supporting these centers should incorporate glycolic acid monitoring in their ethylene glycol screening programs and include analysis of both ethylene glycol and glycolic acid during treatment (hemodialysis) in all confirmed poisonings. Measurement of glycolic acid provides important diagnostic and prognostic information that one cannot correlate with the amount of ethylene glycol in serum or whole blood.

Aged↗
PubMed2004

Comparison of the metabolism of ethylene glycol and glycolic acid in vitro by precision-cut tissue slices from female rat, rabbit and human liver.

1. The metabolism of [1,2-(14)C]-ethylene glycol and [1,2-(14)C]-glycolic acid was studied in vitro using precision-cut tissue slices prepared from the livers of female Sprague-Dawley rats, New Zealand white rabbits and humans. The time-course for production of metabolites formed from ethylene glycol at concentrations from 3 to 40 mM was determined to compare quantitatively the differences between species in the rates and amounts of formation of glycolic acid, the presumed developmental toxicant of ethylene glycol. The rates of metabolism of glycolic acid to glyoxylic acid at concentrations from 0.05 to 16 mM by liver tissue from the different species were also determined. The apparent V(max)/K(m) for the metabolic conversions of ethylene glycol to glycolic acid and for glycolic acid to glyoxylic acid in liver tissue from the different species were obtained. 2. There were qualitative differences in the metabolic profiles and quantitative differences in the formation of glycolic acid between the mammalian liver systems. There was an average of 10-fold less glycolic acid produced by liver slices from rabbits compared with rats. With the human liver, the formation of glycolic acid was not detectable using tissue from three of four human donors. A low level of glycolic acid was detected in one liver slice incubation from one of the four subjects, but only at one extended time point; glyoxylate was detected with liver slices from all four humans. 3. Liver slices prepared from female Sprague-Dawley rats, female New Zealand White rabbits and three female human subjects all metabolized glycolic acid to glyoxylic acid. Human liver tissue was the most effective at further metabolizing glycolic acid to glyoxylic acid. The ratios of V(max)/K(m), representing the relative clearance of glycolic acid from liver tissue, were approximately 14:9:1 for human, rat and rabbit liver, respectively. 4. Precision-cut liver slices maintained in dynamic organ culture are good predictors of metabolism by liver tissue in vivo. The results of the present study therefore indicate that levels of glycolic acid, if formed in vivo, following exposures to similar concentrations of ethylene glycol, would be lower in humans than in rabbits and rats.

Adult↗
PubMed2002

Poly(D,L-lactic acid-co-glycolic acid)-b-poly(ethylene glycol)-b-poly (D,L-lactic acid-co-glycolic acid) triblock copolymer and thermoreversible phase transition in water.

Novel thermoreversible gelation behavior of aqueous solutions of ABA-type triblock copolymers composed of the central polyethylene oxide (PEG) block and two poly(D,L-lactic acid-co-glycolic acid) side blocks was found. Phase transition characteristics, such as critical gel concentration (CGC) and lower and upper critical gel temperature (CGT), are closely related to the molecular structure of the triblock copolymers. The CGC and the lower CGT both increases with increasing PEG/PLGA molecular weight ratio. Increasing the GA content in PLGA block induces a somewhat higher CGC. The copolymer forms micelles with a PLGA loop core and a PEG shell in water. Also grouped micelles are identified seemingly due to the bridging of two micelles sharing two PLGA blocks of a block copolymer chain. As the temperature increases the association of micelles increases, which results in gelation. The ABA-type copolymers exhibit a relatively low CGC (<10%) and low sol-gel transition temperatures compared to BAB-type copolymers. As the temperature increases further gel-sol transition is observed, which would result from the shrinkage of micelles with temperature increase. The hydrodynamic size of the micelles is monitored by dynamic laser scattering, and a possible gelation mechanism was suggested.

Gels↗
PubMed1984

Glycolate causes the acidosis in ethylene glycol poisoning and is effectively removed by hemodialysis.

Six male patients with severe ethylene glycol poisoning were studied with respect to the origin of the metabolic acidosis. The plasma concentrations of ethylene glycol were 4-41 mmol/l and treatment included alkali, ethanol and hemodialysis. Plasma analysis by isotachophoresis and whole blood lactate determinations showed that glycolate (17.0-29.3 mmol/l), lactate (1.4-6.2 mmol/l) and beta-hydroxybutyrate (less than or equal to 1.8 mmol/l) were present in elevated concentrations contributing to the acidosis. Oxalate (less than or equal to 0.33 mmol/l), glyoxylate (less than 0.2 mmol/l) and formate (less than 0.4 mmol/l) concentrations were negligible and did not contribute to any significant degree to the acidosis. The elevated plasma glycolate concentration was highly correlated to the anion gap (r = 0.923) and the glycolate made up for 96.1% (n = 6, range 84.7-108.8) of the increased anion gap. We conclude that glycolate accumulation is the main reason for the metabolic acidosis in ethylene glycol poisoning. The mean dialysator (1.6 m2) clearances of glycolate at a blood flow of 200 ml/min in two patients were 137 ml/min (n = 9, SD +/- 8, range 125-149) and 144 ml/min (n = 11, SD +/- 8, range 133-158). By applying first order kinetics during hemodialysis a volume of distribution of glycolate of 0.55 l/kg was found, assuming that the dialysator clearance equals the total body clearance of glycolate. Thus glycolate, the probable main metabolite of ethylene glycol, is efficiently removed by hemodialysis.

Acidosis↗
PubMed2001

Glycolic acid production using ethylene glycol-oxidizing microorganisms.

Screening for microorganisms oxidizing ethylene glycol to glycolic acid was carried out. Among stock cultures, several yeasts and acetic acid bacteria showed high glycolic acid producing activity. Pichia naganishii AKU 4267 formed the highest concentration of glycolic acid, 35.3 g/l, from 10% (v/v) ethylene glycol (molar conversion yield, 26.0%). Among soil isolates, Rhodotorula sp. 3Pr-126, isolated using propylene glycol as a sole carbon source, formed the highest concentration of glycolic acid, 25.1 g/l, from 10% (v/v) ethylene glycol (molar conversion yield, 18.5%). Rhodotorula sp. 3Pr-126 showed higher activity toward 20% (v/v) ethylene glycol than P. naganishii AKU 4267. Optimization of the conditions for glycolic acid production was investigated using P. naganishii AKU 4267 and Rhodotorula sp. 3Pr-126. Under the optimized conditions, P. naganishii AKU 4267 and Rhodotorula sp. 3Pr-126 formed 105 and 110 g/l of glycolic acid (corrected molar conversion yields, 88.0 and 92.2%) during 120 h of reaction, respectively.

Ethylene Glycol↗
PubMed1993

Hydrogen formation from glycolate driven by reversed electron transport in membrane vesicles of a syntrophic glycolate-oxidizing bacterium.

Oxidation of glycolate to 2 CO2 and 3 H2 (delta G degrees' = +36 kJ/mol glycolate) by the proton-reducing, glycolate-fermenting partner bacterium of a syntrophic coculture (strain FlGlyM) depends on a low hydrogen partial pressure (pH2). The first reaction, glycolate oxidation to glyoxylate (E zero' = -92 mV) with protons as electron acceptors (E zero' = -414 mV), is in equilibrium only at a pH2 of 1 microPa which cannot be maintained by the syntrophic partner bacterium Methanospirillum hungatei; energy therefore needs to be spent to drive this reaction. Glycolate dehydrogenase activity (0.3-0.96 U.mg protein-1) was detected which reduced various artificial electron acceptors such as benzyl viologen, methylene blue, dichloroindophenol, K3[Fe(CN)6], and water-soluble quinones. Fractionation of crude cell extract of the glycolate-fermenting bacterium revealed that glycolate dehydrogenase, hydrogenase, and proton-translocating ATPase were membrane-bound. Menaquinones were found as potential electron carriers. Everted membrane vesicles of the glycolate-fermenting bacterium catalyzed ATP-dependent H2 formation from glycolate (30-307 nmol H2.min-1 x mg protein-1). Protonophores, inhibitors of proton-translocating ATPase, and the quinone analog antimycin A inhibited H2 formation from glycolate, indicating the involvement of proton-motive force to drive the endergonic oxidation of glycolate to glyoxylate with concomitant H2 release. This is the first demonstration of a reversed electron transport in syntrophic interspecies hydrogen transfer.

Adenosine Triphosphatases↗
PubMed1963

GLYCOLIC ACID OXIDATION BY ESCHERICHIA COLI ADAPTED TO GLYCOLATE.

Furuya, Akira (University of Illinois College of Medicine, Chicago) and James A. Hayashi. Glycolic acid oxidation by Escherichia coli adapted to glycolate. J. Bacteriol. 85:1124-1131. 1963.-A procedure is described for extraction and partial purification of glycolic acid oxidase from Escherichia coli adapted to grow on glycolate as the sole carbon source. Enzyme activity was assayed by oxygen uptake and by reduction of 2,6-dichlorophenol-indophenol. Glyoxylic acid was the product of glycolate oxidation by the enzyme. Enzyme activity, which diminishes rapidly on storage, shows a maximum at pH 6 to 7. We were unable to show any cofactor requirement. Compounds which inhibited glycolate oxidation and their order of inhibitory activity were: p-hydroxymercuribenzoate > sodium azide > iodoacetate and o-phenanthroline > ethylenediaminetetraacetic acid. Tests of enzyme specificity showed that the following compounds were oxidized, but at different rates: glycolate, d-lactate, l-lactate, dl-alpha-hydroxybutyrate, dl-malate, and dl-glycerate. Citrate, tartrate, and dl-beta-hydroxybutyrate were not oxidized. Potassium cyanide stimulated oxygen uptake when glycolate and lactate were oxidized. Whether the oxidations were due to different oxidases or to a single oxidase with a wide range of specificities was tested by observing the oxidation of glycolate, d-lactate, and l-lactate under various conditions. Ammonium sulfate fractionation of a crude extract did not change the relative ability to oxidize the three acids. However, the three oxidative capacities diminished at different rates during storage at 0 C for 6 days. The partially purified glycolic oxidase preparations were probably mixtures of several different oxidases.

Azides↗