However, rats exposed for prolonged periods seem to develop chronic renal failure. In the parlance of the street cop, this equates to a blood alcohol level of 0.1%, twice the legal driving limit in Australia. Clin Nephrol. This treatment is only effective in do… It is first converted by alcohol dehydrogenase to glycoaldehyde, which is then metabolised to glycolic acid by aldehyde dehydrogenase. Parry, Michael F., and Ronald Wallach. Typically, people drink this stuff. Effective Treatments for Peripheral Neuropathy, Carpal Tunnel Syndrome Holistic Treatments Ebook, 7 Useful Tips for Improving Your Mental Focus, How to Lose Weight From Your Stomach Fast, An alternative approach to perioral rhytides, Mental Impotence Holistic Treatments Ebook, This substance is a liquid used in antifreeze, paints, polishes and cosmetics. The clinical biochemical features reflect the biochemical and physiological effects. The initial intoxication is thought to occur much in the same way as ethanol intoxication, by acting on the GABA receptors. ", Ethanol for ethylene glycol poisoning [letter. In clinical practice, poisoning with ethylene glycol, methanol, and isopropyl alcohol is common. The treatment options here are discussed in brief. polyethylene glycol. Once past this window of time, absorption has already occurred. Moreau CL, Kerns W, Tomaszewski CA, McMartin KE, Rose SR, Ford MD, Brent J (1998). "Methanol and ethylene glycol poisoning: a case study and review of current literature." It boils at 197 degrees C, in case you ever want to boil some. Thge major interactions of ethylene glycol are with ethanol and fomepizole, which is put to good use in management of the toxicity. This glycolic acid cannot be metabolised in an acid-scavenging way, like lactate or ketones. It and its toxic byproducts first affect the central nervous system, then the heart, and finally the kidneys. Half life is short, but longer with any therapy that blocks the metabolism of ethylene glycol to glycoaldehyde… so with ethanol therapy, the ethylene glycol can hang around for up to 24 hours With therapy, elimination is entirely renal. The lungs show oedema, and occasionally calcium oxalate crystals and degenerative myocardial changes may also occur. Ethylene glycol and its toxic acid metabolytes, "On the metabolic acidosis of ethylene glycol intoxication.". Adolphe Wurtz (1856) "Sur le glycol ou alcool diatomique" (On glycol or diatomic alcohol), Comptes rendus, 43 : 199-204. Competes with ethylene glycol for metabolism via alcohol dehydrogenase (ADH) enzyme. The goal of specific treatment is to prevent the metabolism of ethylene glycol into the toxic metabolites. The major danger is due to its sweet taste, which can attract children and animals. It is not well absorbed through the skin; nor does it evaporate particularly well. It is not well absorbed through the skin; nor does it evaporate particularly well. Such a thing indeed exists, but is not well studied. If untreated, ingestion of only 30 to 60 mls may be sufficient to cause permanent organ damage or death. The elevated NADH to NAD ration causes the conversion of pyruvate pyruvate to lactate. The American Journal of Medicine 57.1 (1974): 143-150. Aldehyde dehydrogenase causes glyceraldhyde to become glycolic acid. Ethylene glycol is moderately toxic, with an oral LDLo = 786 mg/kg for humans. Thus, if you suspect you have accidentally poisoned yourself with ethylene glycol, one may consider four shots of spirits as a rescue therapy. Several deaths are recorded annually in the U.S. alone. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also ex… There are three recogniseable stages to ethylene glycol toxicity. These toxic substances also affect the cardiopulmonary system and can cause renal failure. Conduction disturbances and arrhythmias are to be expected, pulmonary oedema may result from myocardial depression (caused by the acidosis). The acetogenic bacterium Acetobacterium woodii is able to grow by the oxidation of diols, such as 1,2-propanediol, 2,3-butanediol, or ethylene glycol. "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. taste and is readily available it has been used as a poor man's alcohol, but it may also be ingested accidentally and for suicidal purposes. However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. The conversion to glycolic acid is somewhat rapid. The toxic metabolic by-products of ethylene glycol metabolism cause a build-up of acid in the blood (metabolic acidosis). Alternatively, you may consider injecting it. • Supportive care (correct fluid, acid-base, and electrolyte imbalances). 20. Ethylene glycol (EG) poisoning is common in dogs and cats 1 – 4 and often results in death if it is not diagnosed and treated promptly. (See supplemental page for metabolic pathway figures for ethylene glycol and methanol). The consequences of this are as follows: i acidosis due to lactate, oxalate and the other acidic metabolites; this results in metabolic distress and physiological changes ii loss of calcium as calcium oxalate iii deposition of crystals of calcium oxalate in the renal tubules and brain iv inhibition of various metabolic pathways leading to accumulation of organic acids v impairment of cerebral function by oxalate and damage by crystals; also some of the aldehyde metabolites may impair cerebral function vi damage to renal tubules by oxalate crystals leading to necrosis. There is a complex metabolic pathway with multiple products, of which oxalic acid is the most dreaded. The authors (who did not identify themselves) suggested a loading dose of 0.6g per kg body weight, or roughly 40g for a 70kg male, to get to 100mg/dL. c Between 24 and 72 h the kidneys become damaged giving rise to flank pain and acute renal tubular necrosis. META Study Group". Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). The mechanism of metabolic acidosis is more interesting. Moossavi S, Wadhwa NK, Nord EP. However, there is one case series of three poor fools who have admitted to injecting alcohol (ranging from vodka to beer, dosage unknown) and whose veins did not suffer excessively as a consequence, in spite of what i can only assume was suboptimal injecting technique. glucose metabolism, Krebs' cycle, protein synthesis, RNA synthesis and DNA replication for example. Roadmap To Genius Improve Intelligence & IQ, Candida Crusher Permanent Yeast Infection Solution, Glutathione conjugation - Metabolic Activation, Aromatic Hydroxylation - Metabolic Activation, Glucuronide formation - Metabolic Activation, Aliphatic Hydroxylation - Metabolic Activation, How to Cope with Acute Renal Failure Naturally. Like ethanol, ethylene glycol is rapidly absorbed in the GI tract, with peak absorption in 30-60 minutes. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. More bicarbonate must be added in order to buffer the excessive number of hydrogen ions present in the patient, so that H2O and CO2 may be generated. The products of these metabolic pathways are then really eliminated. INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. Both alcohols are metabolised via alcohol dehydrogenase to their toxic metabolites. The parent compound is osmotically active, and is responsible for the increased osmolality observed in the early course of exposure prior to metabolism. Here, we analyzed the metabolism of ethylene glycol. A lot of this information comes from “Goodman & Gilman's The Pharmacological Basis of Therapeutics” 11th ed by Brunton et al,and   “Basic & Clinical Pharmacology” 11th ed. However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. Suppression of metabolism – fomepizole and IV ethanol are temporizing measures; Removal of toxin – haemodialysis; Alkalinisation in order to counteract metabolic acidosis (Na bicarbonate) Folic acid and folinic acid may be useful adjuncts (but does not directly improve patient’s clinical state) Ethylene glycol. One can imagine some sort of cyclical nightmare of ethylene glycol intoxication, ICU admission, discharge and re-intoxication. Ameera S. Mahdi and Andrew J. McBride INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; Alcohol and Alcoholism (1999)  34(6): 918-919. Glycolic acid is further metabolised to glyoxylic acid and oxalic acid. We found that strain JM37 grew rapidly with ethylene glycol as a … GA and EG are currently produced by chemical synthesis, but their biotechnological production from renewable resources has received a substantial interest. EG intoxication is the second most common cause of fatal poisoning in animals according to the American Association of Poison Control Centers. Of the various ways one can become acquainted with ethylene glycol, this is probably the most common. B. Propylene glycol is metabolized to more toxic compounds. Ipecac-induced T he detection of calcium oxalate crystals in the urine is often stated to be a useful guide but this is wrong. The toxicity of ethylene glycol results from its metabolism to more toxic metabolites. The osmolar gap may be raised (to > 10) early in the course but this is variable. These alcohol-related intoxications can present with high anion gap metabolic acidosis and increased osmolality. Partially because lactic acidosis – –The first two steps in ethylene glycol metabolism cause the reduction of NAD to NADH. DEG is used as a component of multiple different products including antifreeze preparations, cosmetics, lubricants, brake fluids, wallpaper strippers, heating/cooling fuel and as a plasticizer. It is only the most common toxin among a  whole family of glycols: Typically, people drink this stuff. Common ethyl alcohol (ethanol) binds much more easily to ADH than ethylene glycol or methanol does. Indications: Ethylene glycol levels > 20 mg/dL DEG has also been inappropriately substituted in pharmaceutical preparations for nontoxic constituents, resulting in more than a dozen epidemics of human poisoning, with resultant … The rationale for the use of bicarbonate is the massive generation of acid by the metabolism of ethylene glycol. Ingestion of sufficient amounts is fatal if untreated. Journal of toxicology. The chief diagnostic feature of ethylene glycol toxicity (apart from doing an actual ethylene glycol level) is calcium oxalate crystals in the urine. Upon ingestion, ethylene glycol is oxidized to glycolic acid, which is, in turn, oxidized to oxalic acid, which is toxic. At this stage, there is no acidosis, but the anion gap is widened (unmetabolised ethylene glycol floods the bloodstream). Potentially, it may interact with things like disulfiram and metronidazole, which block acetaldehyde dehydrogenase. Half life is short, but longer with any therapy that blocks the metabolism of ethylene glycol to glycoaldehyde… so with ethanol therapy, the ethylene glycol can hang around for up to 24 hours, With therapy, elimination is entirely renal. The result of each of the metabolic steps is the production of NADH. The alcohols: ethanol, methanol, isopropanol, ethylene glycol. Metabolism: Ethylene glycol is metabolised in the liver. Glycolic acid (GA) and ethylene glycol (EG) are versatile two-carbon organic chemicals used in multiple daily applications. The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations. Elimination: Ethylene glycol has an elimination half-life of about 3 hours. Fomepizole has an 8,000 fold greater binding affinity to ADH and thus prevents the metabolism of ethylene glycol to toxic acid metabolites. Fig: Metabolism of Ethylene Glycol . The main indication for this (apart from the inevitable renal failure of a late presentation) is a high osmolar gap. N Engl J Med 1981;304:976-8. Methanol and ethylene glycol poisonings share many characteristics both clinically and biochemically. Clay, Keith L., and R. C. Murphy. Ethylene glycol is oxidized via alcohol dehydrogenase into glycoaldehyde, which then undergoes metabolism via aldehyde dehydrogenase into glycolic acid. These 95% commercial antifreeze preparations are diluted ~50% with water when used in vehicle cooling systems. The degeneration of distal tubules may also be seen. As the parent compound, ethylene glycol produces altered mental status similar to ethyl alcohol. Central nervous system depression is the most pronounced feature at this stage; the coma may be garnished with seziures. Mono Ethylene Glycol, commonly referred to as Ethylene Glycol Antifreeze but also referred to as Ethane-1,2-diol, MEG, EG and Industrial Glycol. In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting step in the metabolism of ethylene glycol. b intravenous sodium bicarbonate; this corrects the acidosis—animal studies have shown that this increases the LD50 by around four times c calcium gluconate; this corrects the hypocalcaemia d dialysis to remove ethylene glycol. As it has a sweet. Some redness and burning at the site were the only reported side effects. "On the metabolic acidosis of ethylene glycol intoxication." Ethylene glycol is a precursor for many polymers, eg. Diethylene glycol was once used as a vehicle for the drug sulphanilamide and when used for this it caused some 76 deaths. The next stage is that of cardiac toxicity. If ingestion was recent (1-2 hours), vomiting is induced and activated charcoal is given to reduce further absorption of the ethylene glycol. Ethanol for ethylene glycol poisoning [letter]. Crystals, blood and protein may all be detected in the urine (crystalluria, haematuria and proteinuria, respectively), and the urine may have a low specific gravity. The investigation of its microbial metabolism therefore provides insights into the environmental fate of this pollutant and also enables its utilization … Hypocalcemia may occur as oxalate chelates the serum calcium. Pediatr Clin North Am. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benefit unless it is performed within 60 minutes of ingestion. Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning. In 1977, Clay and Murphy poisoned some monkeys and revealed that the serum bicarbonate levels decreased in proportion to rising glycolic acid levels. Methanol and ethylene glycol metabolism can be understood by first studying the metabolism of ethanol, which occurs in two steps: Ethanol is oxidized to acetaldehyde with production of NADH by alcohol dehydrogenase, an enzyme located, for the most part, in the cytosol of hepatocytes (see Chapter 24 ). Thus the pathological damage includes cerebral oedema, haemorrhage and deposition of calcium oxalate crystals. Most intoxications are associated with ingestion of antifreeze, which is typically 95% EG. Ethylene glycol is rapidly absorbed from the gastrointestinal tract and slowly absorbed through the skin or lungs. Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). There is degeneration of proximal tubular epithelium with calcium oxalate crystals and fat droplets detectable in tubular epithelial cells. By Katzung et al. It does what ethanol would do, except it does so with great expense, and without ethanol intoxication. Litovitz T. More than 6 per cent of poisonings involve alcohols and glycols, reflecting their availability in a wide range of household products, including aftershave, brake fluid, gas line antifreeze, model airplane fuel, mouthwash, rubbing alcohol, and windshield washing solution. Thus the treatment of poisoning with ethylene glycol is a logical result of understanding the biochemistry of the toxicity. Recent analyses demonstrated fundamentally different ways for oxidation of 1,2-propanediol and 2,3-butanediol. DePass LR, Garman RH, Woodside MD, Giddens WE, Maronpot RR, Weil CS. This deliciously syrupy tongue-pleasing alcohol is a favourite among the critically ill population. C. Ethylene glycol is … 1986 Nov;7(4):547-65. The most important initial treatment for ethylene glycol poisoning is stabilizing the person. Methanol is slowly metabolised to formaldehyde which is rapidly metabolised to formate, the metabolite mainly resp … Alcohol dehydrogenase, the same first step enzyme responsible for the metabolism of methyl and ethyl alcohols, slowly catalyzes conversion of EG to glycoaldehyde. Thus, after standard procedures such as gastric lavage to reduce absorption and supportive therapy for shock and respiratory distress, patients are treated with the following: a ethanol; this competes with ethylene glycol for alcohol dehydrogenase, but as it is a better substrate the first step in ethylene glycol metabolism is blocked—animal studies have shown that this doubles the LD50. Ethylene Glycol was first formulated in the 1850’s and is now commercially produced through a chemical reaction between Ethylene Oxide and a catalyst. Both susbtances are well removed by dialysis, and on top of that one can adjust the bicarbonate concentration of the dialysate to donate extra bicarbonate to the patient's bloodstream, increasing the correction of the acidosis even further. The first step is catalysed by the enzyme alcohol dehydrogenase and herein lies the key to treatment of poisoning. Henderson, William R., and Jeffrey Brubacher. After about 36-48 hrs, the renal failure becomes the dominant feature. Also, the intermediate metabolites of ethylene glycol have metabolic effects such as the inhibition of oxidative phosphorylation. Biotransformation studies have been performed to understand why ethylene glycol causes toxic effects. I cannot find the original paper, but a letter in response to it suggests one should sustain a blood ethanol concentration of 20 to 30 mmol/L (100 to 150 mg/dL). How drunk do you have to be to prevent ethylene glycol metabolism? Ethylene glycol is more toxic to humans than animals, and in general the susceptible species are those which metabolize the compound to oxalic acid, although this is quantitatively a minor route. First you may feel slightly drunk for about 4 hours. 5 The mortality rate in dogs is reported to range from 59% to 70% 1, 5 and is thought to be even higher in cats. In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. Glycolic acid is the smallest of the alpha-hydroxy acids, and is used in all sorts of skin-related industries (be it tanning, as a leather-dye, or as a part of dermatological skin peeling). 2003 Sep;60(3):205-10. This increases its clearance, and keeps it out of the fatty central nervous system, where its effects are the most destructive (specifically, the effects on the tender juicy retina). Cjem 4.1 (2002): 34-40. 1986 Apr;33(2):311-23. To summarize, you give massive amounts of bicarbonate, and then you either start an ethanol infusion, regular doses of fomepizole, or haemodialysis. Then, you might feel slightly ill. As the glycolic acid begins to appear in the bloodstream, metabolic acidosis ensues and hyperventilation follows. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also excreted by the unhappy kidneys (which find themselves mangled by the process). OVERVIEW >1 mL/kg or a mouthful in a child is potentially lethal ethylene glycol itself is relatively non-toxic -> metabolites extremely toxic (glycolate) rate limiting step = alcohol dehydrogenase activity accumulation of glycolate -> direct cellular toxicity CLINICAL FEATURES drunk: automotive antifreeze, solvent, polish, paints, cosmetics, brake fluid, car wash fluid. Certainly. Good old alcohol, in large quantities, will overwhelm alcohol dehydrogenase, saturating it. Chronic toxicity and oncogenicity studies of ethylene glycol in rats and mice. All animals are susceptible to ethylene glycol (EG) toxicity, but it is most common in dogs and cats. The treatment of poisoning with ethylene glycol reflects the mechanism and biochemical effects. Ethylene glycol, the parent compound, is inebriating but generally considered nontoxic. Diethylene glycol (DEG) is a clear, colorless, odorless liquid with a sweet taste, and is an excellent solvent for water-insoluble chemicals and drugs. Apparently, it gives one a buzz similar to that of alcohol intoxication. Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. ternative metabolism of toxic alcohols to non-toxic metabolites. There is a lot of good, thorough literature on the management of ethylene glycol toxicity. Previous chapter: Urate and hippurate anions: their origins and clearance, Next chapter: Diabetic, alcoholic and starvation ketoacidosis. META Study Group". In patients exposed to ethylene glycol, 100mg thiamine and 100mg pyridoxine can be administered IV daily Pollution from ethylene glycol, and plastics containing this monomer, represent a significant environmental problem. "Ethylene glycol poisoning." "Methanol and ethylene glycol poisoning: a case study and review of current literature. Chronic toxicity and oncogenicity studies of ethylene glycol in rats and mice. This is mainly because A. Absorption of propylene glycol from the gastrointestinal tract is slow. b Between 12 and 24 h there is tachypnoea, tachycardia, hypertension, pulmonary oedema and congestive cardiac failure. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. 4-Methylpyrazole, or fomepizole as it is known, is basically a competitive antagonist to alcohol dehydrogenase. This effect rarely produces serious morbidity or death by itself.Acute renal failure as well as a severe anion-gap metabolic acidosis results from the metabolism of ethylene glycol into at least 4 distinct metabolites. The imbalance in the level of this in the body is adjusted by oxidation to NAD coupled to the production of lactate. Fundam Appl Toxicol. Pure ethylene glycol is said to be sweet-tasting, but nowadays (in order to deter children, one assumes) the majority of it is tainted with foul-tasting impurities. We found that strain JM37 grew rapidly with ethylene glycol as a sole source of carbon and energy, while strain KT2440 did not grow within 2 days of incubation under … There are two proposed mechanisms of propylene glycol metabolism: The first is as follows: Ethylene glycol is transformed in the liver by alcohol dehydrogenase to glyceraldehyde. The minimum lethal dose of ethylene glycol is about 100 ml and after ingestion death may occur within 24 h from damage to the CNS or more slowly (8-12 days) from renal failure. The highest survived dose reported is 2 litres. Clinical toxicology 36 (7): 659–66. An additional benefit is the effect of "ion trapping" formic acid. 1. The extra osmoles represent some mixture of ethylene glycol and glycolic acid, eagerly water-soluble, and thus rapidly dialysed. Anything over 0.1ml/kg will require treatment. Anything over 1.0-1.5mg/kg is considered lethally toxic. Lactate gap refers to the difference in lactate measurement via different methods: Elevated lactate on portable blood gas machine utilizing lactate oxidase. 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. Supportive therapy, such as IV fluids, is also important. Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. Thus, there is reduced plasma bicarbonate, low plasma calcium and raised potassium. Neither as exciting as intravenous alcohol, nor as expensive as fomepizole, continous veno-venous haemodiafiltration is the method of choice for getting rid of huge quantities of ethylene glycol rapidly. Ethylene glycol metabolism generates glycolate, which can be mistaken for lactate by portable lab assays utilizing lactate oxidase. In contrast to ethylene glycol, propylene glycol rarely causes toxic effects. Thus, this acidosis is "bicarbonate-resistant". There is thus an increase in the level of lactate and lactic acidosis may result. Permanent optic atrophy may occur. Compared to ethylene glycol, ethanol had something like 100 times more affinity for alcohol dehydrogenase. The rate-limiting step of ethylene glycol metabolism is the ADH-catalyzed step. Only at the third admission, 2 years after the first, was the possibility of an underlying metabolic disorder considered. The result is a failure to convert ethylene glycol into glycoaldehyde; ethylene glycol remains in the circulation, gradually (and harmlessly) being excreted into the urine. There seem to be three recognizable clinical stages: a Within 30 min and lasting for perhaps 12 h, there is intoxication, nausea, vomiting, coma, convulsions, nystagmus, papilloedema, depressed reflexes, myoclonic jerks and tetanic contractions. The contribution of all the other metabolites was negligible. A Norfolk couple report that it tasted "horrible", though the husband finished his glass as a demonstration of his manliness. Toxicology and applied pharmacology 39.1 (1977): 39-49. Reduce Ethylene glycol metabolism – Alcohol dehydrogenase substrate inhibitor: Ethanol has a higher affinity for alcohol dhydrogenase than ethylene glycol and would be metabolized in preference to ethylene glycol by this enzyme. In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. 1) 4-methylpyrazole (4-MP)[Antizole or fomepazole]: This medication inactivates alcohol dehydrogenase. The typical way to administer alcohol in such a situation is to give it via a central vein (it being such a good peripheral venous sclerosant that it is in fact routinely injected into varicose veins to destroy them). As a weak acid, formic acid should become more water soluble in an alkaline bloodstream, and in alkaline urine. On the first admission, glycolic acid was detected in his blood and he was diagnosed as having ethylene glycol intoxication. 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