Glycolic Acid Levels Research Articles

GC-MS Based Metabolic Profiling of Parkinson's Disease with Glutathione S-transferase M1 and T1 Polymorphism in Tunisian Patients.

Parkinson's disease (PD) is the second most common neurodegenerative disease. It is a multifactorial disorder (caused by aging, environmental, and genetic factors). Metabolomics can help explore the biomarker profiles for aging. Recent studies showed an association between the glutathione S-transferases (GSTs) polymorphisms and PD risk. The purpose of this study was to evaluate the association of this genetic polymorphism and the metabolomic profile in PD Tunisian patients, in order to identify effective biomarkers in the genetic differentiation. In this study, the metabolomic profile changes related to GSTs polymorphism were searched in 54 Tunisian PD patients treated with L-dopa, using a gas chromatography-mass spectrometry (GC-MS) technique. The study results showed that mannose, methyl stearate, and three other unknown metabolites, increased in patients with GSTM1 positive genotype, while glycolic acid, porphine, monomethyl phosphate, fumaric acid, and three other unknown metabolites decreased in patients with GSTM1 positive genotype. Subsequently, the levels of glycolic acid, erythronic acid, lactic acid, citric acid, fructose, stearic acid, 2-amino-2-methyl-1,3-propanediol and three other unknown metabolites increased in patients with GSTM1 positive genotype, while the levels of proline, valine and two unknown metabolites decreased with GSTT1 positive genotype. All these altered metabolites are related to energy metabolism and it can be concluded that GSTs polymorphism based the shifting in energy metabolism and led to oxidative stress.

320-LB: Metabolically Unhealthy Overweight Individuals Have High Lysophosphatide Levels, Phospholipase Activity, and Oxidative Stress

Background and Aims: Metabolically unhealthy overweight (MUO) individuals and metabolically healthy overweight (MHO) individuals differ in biomarkers of atherogenesis. Metabolomic approaches enable studies of the metabolic variables underlying these differences. Methods: We determined the metabolomes in plasma samples from 34 MUO and 34 MHO individuals matched for sex, age, and body mass index (BMI) to identify potential metabolic markers or pathways associated with atherogenic traits. Results: This analysis revealed that the MUO group had significantly higher levels of glycolic acid, 6 lysophosphatidylethanolamines (lysoPEs), and 12 lysophosphatidylcholines (lysoPCs). Although the two groups had similar total body fat percentages and lean body masses, MUO individuals had larger visceral fat areas (VFAs). They also had greater circulating lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and higher levels of oxidized low-density lipoprotein (ox-LDL) and urinary 8-epi-prostaglandin F2α (8-epi-PGF2α), reflecting higher risks for oxidative and lipid-related tissue damage. The following measures were positively correlated: VFA and ox-LDL; ox-LDL and Lp-PLA2 activity; and lysoPC, lysoPE, and 8-epi-PGF2α levels. Chronic plasma lysoPC increases were associated with atherogenic traits, higher levels of mean ox-LDL, 8-epi-PGF2α, Lp-PLA2, and visceral fat accumulation in MUO compared to MHO individuals. Conclusions: This panel of plasma metabolites distinguishes MUO from MHO individuals and will enable future research on fat dysregulation and obesity. Disclosure Y. Han: None. M. Kim: None. H. Yoo: None. J. Lee: None. Funding National Research Foundation of Korea (NRF-2017R1C1B2007195, NRF-2012M3A9C4048762)

Metabolically unhealthy overweight individuals have high lysophosphatide levels, phospholipase activity, and oxidative stress

Metabolically unhealthy overweight (MUO) individuals and metabolically healthy overweight (MHO) individuals differ in biomarkers of atherogenesis. Metabolomic approaches enable studies of the metabolic variables underlying these differences. We determined the metabolomes in plasma samples from 34 MUO and 34 MHO individuals matched for sex, age, and body mass index (BMI) to identify potential metabolic markers or pathways associated with atherogenic traits. This analysis revealed that the MUO group had significantly higher levels of glycolic acid, 6 lysophosphatidylethanolamines (lysoPEs), and 12 lysophosphatidylcholines (lysoPCs). Although the two groups had similar total body fat percentages and lean body masses, MUO individuals had larger visceral fat areas (VFAs). They also had greater circulating lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and higher levels of oxidized low-density lipoprotein (ox-LDL) and urinary 8-epi-prostaglandin F2α (8-epi-PGF2α), reflecting higher risks for oxidative and lipid-related tissue damage. The following measures were positively correlated: VFA and ox-LDL; ox-LDL and Lp-PLA2 activity; and lysoPC, lysoPE, and 8-epi-PGF2α levels. Chronic plasma lysoPC increases were associated with atherogenic traits, higher levels of mean ox-LDL, 8-epi-PGF2α, Lp-PLA2, and visceral fat accumulation in MUO compared to MHO individuals. This panel of plasma metabolites distinguishes MUO from MHO individuals and will enable future research on fat dysregulation and obesity.

A molecular dynamics simulation study on the mechanism of loading of gemcitabine and camptothecin in poly lactic-co-glycolic acid as a nano drug delivery system

The poly lactic-co-glycolic acid copolymer has become one of the most widely used synthetic macromolecules available for use in nanoscale drug delivery studies because of its biocompatibility and biodegradability. In this study, using computational molecular dynamics methods, combinations of polymer with different amounts of lactic and glycolic acid were compared for loading hydrophilic and hydrophobic of Gemcitabine and Camptothecin. These simulations were carried out in different ratios of the drug to the polymer. The results show that in all monomeric ratios, the amount of Camptothecin loading is higher, but on the other hand, the energy of the interaction of Gemcitabine with copolymer is greater, which can reduce its release rate from the system. By increasing the amount of glycolic acid in its system, it's the flexibility is increased and the formation of nanoparticles is also increased. Increasing the formation of nanoparticles leads to increase of the amount of drug loading of Gemcitabine. Conversely, with the increase in lactic acid content, the polymer's flexibility is diminished due to methyl group steric hindrance and the formation of nanoparticles is impaired. The results also show that for the formation of polymersomes, the drugs are first attached to the polymers, and then these compounds form the final nanoparticles as close as possible. Finally, this study suggests that poly lactic-co-glycolic acid is more suitable for loading hydrophobic drugs in any ratio of monomers. However, with increasing glycolic acid levels, its ability to load hydrophilic drugs also reaches a reasonable level.

Determination of glycolic acid in natural seawater by liquid chromatography coupled with triple quadrupole mass spectrometry

AbstractGlycolic acid, which is produced during photorespiration, is one of the major components of dissolved organic matter released by phytoplankton, comprising up to 40% of their daily primary productivity. However, the sensitivity of existing methods does not allow for accurate measurement of glycolic acid levels in oligotrophic seawater. In this study, we present a straightforward, robust, and sensitive liquid chromatography‐mass spectrometry (LC‐MS) method to quantify glycolic acid in natural seawater following liquid‐liquid extraction, requiring only a small sample size (25 mL seawater). The method has a highly sensitive detection limit of 9 nM, at least fivefold lower than existing methods. This approach was successfully applied to the analysis of seawater samples collected from both eutrophic and oligotrophic marine environments. The results showed that glycolic acid concentrations in natural seawater are positively correlated with chlorophyll a concentrations, indicating that phytoplankton contribute significantly to glycolic acid production in marine environments. As glycolic acid is an important carbon and energy source for marine bacteria, the method developed within this study allows further investigation into the rates of its release and uptake by phytoplankton and heterotrophic bacteria, respectively, as well as the role it plays in phytoplankton–bacteria interactions.

Metabolic Differentiation of Diamondback Moth (Plutella xylostella (L.)) Resistance in Cabbage (Brassica oleracea L. ssp. capitata)

The diamondback moth, Plutella xylostella (L.), is a major pest responsible for destroying cabbage and other Brassica vegetable crops. A diamondback moth-resistant cabbage line was studied by comparing its metabolite profiles with those of a susceptible cabbage. Fourier transform infrared spectroscopy analysis revealed that carbohydrates, aromatic compounds, and amides were the major factors that distinguished the resistant and susceptible genotypes. Gas chromatography-time-of-flight mass spectrometry profiled 46 metabolites, including 19 amino acids, 15 organic acids, 8 sugars, 3 sugar alcohols, and 1 amine in two genotypes and F1 hybrid cabbages. The levels of glycolic acid, quinic acid, inositol, fumaric acid, glyceric acid, trehalose, shikimic acid, and aspartic acid were found to be very significantly different between the resistant and susceptible genotypes with a P value of <0.0001. These results will provide a foundation for further studies on diamondback moth resistance in cabbage breeding and for the development of other herbivore-resistant crops.

The Impact of Dose Rate on Ethylene Glycol Developmental Toxicity and Pharmacokinetics in Pregnant CD Rats

High-dose bolus exposure of rats to ethylene glycol (EG) causes developmental toxicity mediated by a metabolite, glycolic acid (GA), whose levels increase disproportionately when its metabolism is saturated. However, low-level exposures that do not saturate GA metabolism have a low potential for developmental effects. Toward the goal of developing EG risk assessments based on internal dose metrics, this study examined the differences between fast (bolus) and slow (continuous infusion) dose-rate exposures to EG on developmental outcome and pharmacokinetics. Time-mated female CD rats received sc bolus injections of 0, 1000, or 2000 mg/kg/day of EG on gestation day (GD) 6-15 once daily, whereas three corresponding groups were given the same daily doses as an infusion administered continuously from GD 6-15 via an sc implantable pump. In the sc bolus groups, increases in 11 fetal malformations (major defects) and 12 variations (minor alterations) were seen at the 2000 mg/kg/day dose level, whereas increases in 2 malformations and 2 variations occurred at 1000 mg/kg/day. In contrast, equivalent daily doses of EG given slowly via infusion did not cause any developmental effects. A pharmacokinetics time course was then conducted to compare GD 11-12 kinetics from oral bolus (gavage) exposure versus sc infusion of EG. Although dose rate had a modest impact (8- to 11-fold difference) on peak EG levels, peak levels of GA in maternal blood, kidney, embryo, and exocoelomic fluid were 59, 100, 49, and 56 times higher, respectively, following gavage versus the same dose given by infusion. These data illustrate how high-dose bolus exposure to EG causes a dramatic shift to nonlinear GA kinetics, an event which is highly unlikely to occur following exposures to humans associated with consumer and worker uses.

Ethylene Glycol and Glycolic Acid in Postmortem Blood from Fatal Poisonings

Ethylene glycol (EG), a relatively infrequent cause of fatal intoxication, presents an analytical challenge for forensic confirmation in postmortem toxicology. We report EG and glycolic acid (GA) quantification in postmortem blood by gas chromatography coupled with ion trap mass spectrometry (GC-MS) analysis using a modification of a previously reported clinical method. The method is linear from 50 to 4000 mg/L with a limit of detection of 25 mg/L for both EG and GA. Interassay coefficient of variation (2.1-8.6%, 4.3-6.0%) and accuracy (96-101%, 92-105%) were determined for EG and GA, respectively. EG concentration by ion trap GC-MS correlated closely (R(2) = 0.995) with EG quantified by GC-flame-ionization detection. Analysis of blood from 20 autopsies with no evidence of EG exposure did not reveal detectable EG or GA. In 12 medical examiner cases with EG poisoning as cause of death, EG concentrations ranged widely from 58 to 7790 mg/L with a mean of 1830 mg/L, and the GA concentration averaged 1360 mg/L with a narrower range of 810-1770 mg/L. EG and GA levels correlate poorly (R(2) = 0.15) in postmortem blood with discordantly low EG concentrations in two cases. Birefringent oxylate crystals in renal tissue was a consistent finding. In conclusion, a sensitive and specific GC-MS method for detection and quantification of EG and GA has been validated and a study of fatal EG poisonings revealed forensic application of the method.

Species‐specificity of ethylene glycol‐induced developmental toxicity: toxicokinetic and whole embryo culture studies in the rabbit

High-dose gavage exposure to ethylene glycol (EG) is teratogenic in rats, but not rabbits. To investigate the reason for this species difference, toxicokinetic and whole embryo culture (WEC) studies were conducted in gestation day 9 New Zealand White rabbits, and the data compared to very similar data previously generated in pregnant rats. In the toxicokinetic study, maximal levels of unchanged EG in rabbits were comparable to those reported for rats. However, maximal levels of EG's teratogenic metabolite, glycolic acid (GA), in rabbit maternal blood and embryo were only 46% and 10% of the respective levels in rats. The toxicokinetic profile suggested that the lower GA levels in rabbits were due to a slower rate of maternal metabolism of EG to GA, slow uptake of GA into the yolk sac cavity fluid which surrounds the embryo, and negligible transfer via the visceral yolk sac (VYS) placenta. In the WEC study, exposure of rabbit conceptuses to high concentrations (< or = 12.5 mM) of GA was without effect, which contrasts with reported effects in rat WEC at > or = 3 mM. Overall, these data implicate toxicokinetics as an important factor underlying the species difference, although intrinsic insensitivity of the rabbit embryo might also be involved. Integration of these findings with published human data suggest that the rabbit is the more relevant model for human EG exposure, based on the negligible role of the rabbit VYS in placental transfer (humans lack a VYS) and similar rates of EG metabolism and extraembryonic fluid turnover.

Lactate gap and ethylene glycol poisoning

Lactate gap and ethylene glycol poisoning

Development of a Physiologically Based Pharmacokinetic Model for Ethylene Glycol and Its Metabolite, Glycolic Acid, in Rats and Humans

An extensive database on the toxicity and modes of action of ethylene glycol (EG) has been developed over the past several decades. Although renal toxicity has long been recognized as a potential outcome, in recent years developmental toxicity, an effect observed only in rats and mice, has become the subject of extensive research and regulatory reviews to establish guidelines for human exposures. The developmental toxicity of EG has been attributed to the intermediate metabolite, glycolic acid (GA), which can become a major metabolite when EG is administered to rats and mice at high doses and dose rates. Therefore, a physiologically based pharmacokinetic (PBPK) model was developed to integrate the extensive mode of action and pharmacokinetic data on EG and GA for use in developmental risk assessments. The resulting PBPK model includes inhalation, oral, dermal, intravenous, and subcutaneous routes of administration. Metabolism of EG and GA were described in the liver with elimination via the kidneys. Metabolic rate constants and partition coefficients for EG and GA were estimated from in vitro studies. Other biochemical constants were optimized from appropriate in vivo pharmacokinetic studies. Several controlled rat and human metabolism studies were used to validate the resulting PBPK model. When internal dose surrogates were compared in rats and humans over a broad range of exposures, it was concluded that humans are unlikely to achieve blood levels of GA that have been associated with developmental toxicity in rats following occupational or environmental exposures.

Successful transplantation of a liver from a donor with fatal ethylene glycol poisoning

Successful transplantation of a liver from a donor with fatal ethylene glycol poisoning

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 [1,2-14C]-ethylene glycol and [1,2-14C]-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 VmaJKm 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 F"max/-/Cm, 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 concentrationsof ethylene glycol, would be lower in humans than in rabbits and rats.

Major factors modulating the serum oxalic acid level in hemodialysis patients.

Ascorbic acid overload and vitamin B6 deficiency have been implicated in the development of hyperoxalemia in dialysis patients, but there is still disagreement about this. Hemodialysis patients who are exposed long-term hyperoxalemia may develop secondary oxalosis with an increased risk of cardiac, vascular, and bone disease, and thus may benefit from maintaining a low serum oxalic acid level. In 452 hemodialysis patients, the serum level of oxalic acid was 47.2 +/- 22.9 micromol /l before and 16.9 +/- 10.5 micromol/l after a 4-hour dialysis session, while the ascorbic acid levels were 39.0 +/- 92.7 micromol/l and 6.5 +/- 18.6 micromol/l, the glycolic acid levels were 7.3 +/- 10.1 micromol/l and 0.6 +/- 2.3 micromol/l, and the citric acid levels were 141.3 +/- 54.7 micromol/l and 117.6 +/- 37.2 micromol/l, respectively. Most patients (65.3 percent) had low serum ascorbic acid levels (less than 10 micromol/l) before hemodialysis. The serum level of oxalic acid [Ox] showed a significant positive correlation with the levels of ascorbic acid [AA], glycolic acid [Gly], and creatinine [Cre]: [Ox] = 21.711 + 0.181 x [AA] + 0.174 x [Gly] + 0.171 x [Cre], (all micromol/l, p less than 0.05). In 124 dialysis patients, the 4-pyridoxic acid level was 8.9 +/- 19.6 micromol /l before and 3.9 +/- 8.8 micromol/l after dialysis, and it was not correlated with oxalic acid or glycolic acid. Most dialysis patients (65.3 percent) had low serum levels of ascorbic acid, but a subgroup of patients (12 percent) had high serum ascorbic acid levels (more than 100 micromol/l) associated with hyperoxalemia (88.2 +/- 24.5 micromol/l). High-dose vitamin C supplementation may aggravate hyperoxalemia in hemodialysis patients, so attention should be paid to avoiding this risk.

Dose-dependent nonlinear pharmacokinetics of ethylene glycol metabolites in pregnant (GD 10) and nonpregnant Sprague-Dawley rats following oral administration of ethylene glycol.

The kinetics of orally administered ethylene glycol (EG) and its major metabolites, glycolic acid (GA) and oxalic acid (OX), in pregnant (P; gestation day 10 at dosing, GD 10) rats were compared across doses, and between pregnant and nonpregnant (NP) rats. Groups of 4 jugular vein-cannulated female rats were administered 10 (P and NP), 150 (P), 500 (P), 1000 (P), or 2500 (P and NP) mg (13)C-labelled EG/kg body weight. Serial blood samples and urine were collected over 24-hr postdosing, and analyzed for EG, GA, and OX using GC/MS techniques. Pharmacokinetic parameters including Cmax, Tmax, AUC, and betat((1/2)) were determined for EG and GA. Pregnancy status (GD 10-11) had no impact on the pharmacokinetic parameters investigated. Blood levels of GA were roughly dose-proportional from 10 to 150 mg EG/kg, but increased disproportionately from 500 to 1000 mg EG/kg. EG and GA exhibited dose-dependent urinary elimination at doses > or = 500 mg EG/kg, probably due to saturation of metabolic conversion of EG to GA, and of GA to downstream metabolites. The shift to nonlinear kinetics encompassed the NOEL (500 mg EG/kg) and LOEL (1000 mg EG/kg) for developmental toxicity of EG in rats, providing additional evidence for the role of GA in EG developmental toxicity. The peak maternal blood concentration of GA associated with the LOEL for developmental toxicity in the rat was quite high (363 microg/g or 4.8 mM blood). OX was a very minor metabolite in both blood and urine at all dose levels, suggesting that OX is not important for EG developmental toxicity.

An investigation into the effects of residual water on the glass transition temperature of polylactide microspheres using modulated temperature DSC.

The objective of the study was to ascertain residual water levels in polylactide and polylactide-co-glycolide microspheres prepared using the solvent evaporation technique and to investigate the effects of that water on the glass transitional behaviour of the microspheres. Microspheres were prepared from polylactic acid (PLA) and polylactide-co-glycolide (PLGA) 50:50 and 75:25 using a standard solvent evaporation technique. The glass transition was measured as a function of drying conditions using modulated temperature DSC. The microspheres were found to contain very low levels of dichloromethane, while residual water levels of up to circa 3% w/w were noted after freeze or oven drying, these levels being higher for microspheres containing higher glycolic acid levels. The residual water was found to lower the T(g) following the Gordon-Taylor relationship. The data indicate that the microparticles may retain significant water levels following standard preparation and drying protocols and that this drying may markedly lower the T(g) of the spheres.

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

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. 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. 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. 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.

Synthesis of yttria-doped strontium-zirconium oxide powders via ammonium glycolate combustion methods as precursors for dense ceramic membranes

Ammonium glycolate combustion was used to synthesize SrZr0.95Y0.05O3 − x powders. Soluble metal-glycolate complexes, detected by infrared spectroscopy, were formed with Y+3 and Zr+4, which maintain atomic level mixing of metal cations with glycolic acid. Sr+2/glycolic acid mixtures did not form glycolate complexes. Temperature-programmed reaction studies showed that only precursor solutions with metal-glycolate complexes combust, indicating that the combustion is initiated by metal-glycolate complexes. Varying the ammonium hydroxide content and glycolic acid levels above that required to form glycolate complexes did not affect surface area and crystallinity. Decreasing the glycolic acid/nitrate ratio increases the temperatures reached during combustion. Thick disks prepared from co-precipitated and ammonium glycolate powders demonstrated that combustion synthesized powders reach higher densities. Surface area and SEM indicated that the ammonium glycolate powders have smaller particle sizes, which favor densification, than co-precipitated powders.

Induction of Voluntary Feed Intake Restriction in Broiler Chicks by Dietary Glycolic Acid Supplementation

Experiments were conducted to evaluate the effects of feeding various dietary levels of glycolic acid (GA) on feed intake (FI) and growth in young broiler chickens. When fed at a supplementation level equimolar to glycine (GLY, 2.64% of the diet), chicks fed GA consumed 44% less feed from 21 to 42 days of age than those fed GLY, and 25% less than those fed an equimolar level of glyoxylic acid. Graded dietary levels of GA (0 to 3% of the diet) were fed in additional experiments to chicks from 0 to 14, 0 to 21, or 21 to 42 days of age, respectively. In all three age periods, a dose-dependent reduction in FI was observed with GA supplementation. In only one experiment at the highest level (3%) did dietary GA significantly increase mortality. Acetic acid supplementation (1.7 and 3.4% of the diet), unlike supplementation with equimolar levels of GA, had no influence on FI. Glycolic acid has potential as a chemical means of restricting voluntary FI in avian species where this is necessary for obtaining optimum reproductive efficiency, reduced fat deposition, or cessation of egg production.