Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old man with arterial hypertension suffered from depression and suicidal wish after a cerebrovascular accident and transitory left hemiparesis. He was urgently admitted to hospital in severe metabolic acidosis which caused renal failure and coma, ending fatally within two days. At necropsy calcium oxalate crystals were found in the renal tubules and cerebral vessel walls with chemically induced meningoencephalitis. From these findings glycol poisoning was diagnosed. There was a lethal concentration of ethylene glycol in the urine. The toxic effects of ethylene glycol are due to its metabolites. The oxalate crystals are primarily of diagnostic importance.
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PMID:[Ethylene glycol poisoning]. 337 4

The purpose of this investigation was to compare the effects of ethanol and 4-methylpyrazole (4MP) on the toxicity and pharmacokinetics of ethylene glycol (EG) in the dog. All dogs received 173 mmol/kg EG, p.o. Dogs were randomly assigned to 3 groups: EG-treated only, EG + ethanol (19.3 mmol/kg, i.v. 3, 7, 14 and 24 h after EG) and EG + 4MP (0.24 mmol/kg, i.v. 3 h after EG, 0.18 mmol/kg at 24 h and 0.06 mmol/kg at 36 h). EG produced a rapid onset of metabolic acidosis (within 3 h) and acute oliguric renal failure (after 48 h), whereas administration of ethanol or 4MP greatly attenuated acidosis and prevented renal toxicity. The administration of ethanol, however, severely increased the central nervous system (CNS) depression that existed after ingestion of EG. The half-life of FG in serum was 10.8 +/- 0.7 h in the EG-only treatment group, 6.8 +/- 0.7 (P less than 0.05) in the EG + ethanol group and 9.8 +/- 0.9 h in the EG + 4MP group. Approx. 10% and 48% of the dose of EG was excreted unchanged in the urine at the 0-3 and 3-72 h periods, respectively. Treatment with 4MP increased the amount of EG excreted in the urine (71% from 3-72 h), whereas ethanol did not (51%). However, both ethanol and 4MP increased the rate constant of EG excretion into urine approx. 70%. These data demonstrate the utility of 4MP over ethanol for the treatment of EG-induced toxicity in dogs and indicate that ethanol and 4MP cause an increase in the rate constant of EG excretion in the urine and not a prolongation in EG half-life.
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PMID:Comparison of the effects of ethanol and 4-methylpyrazole on the pharmacokinetics and toxicity of ethylene glycol in the dog. 382 18

1. Rat kidney cortical slices, with metabolism suppressed by iodoacetate, were incubated anaerobically at 26 degrees C in hyperosmotic saline media. Changes in tissue composition with time, up to 12 hr, were studied. Despite initial shrinkage, gross swelling occurred, even in saline media of more than twice the concentration of normal extracellular fluid.2. The composition of non-metabolizing kidney slices incubated at 26 degrees C in a balanced saline medium containing 7 g polyethylene glycol 6000 (PEG 6000)/100 ml. was determined at intervals up to 12 hr. The tissue water, sodium and chloride contents had reached constant levels by 6 hr. Potassium continued to leak slowly from the tissue, but there was no significant further loss between 10 and 12 hr.3. Non-metabolizing kidney slices were incubated in PEG medium containing additional quantities of either a non-electrolyte (400 m-osmole glucose/kg H(2)O) or an electrolyte (400 m-osmole NaCl/kg H(2)O), both of which penetrated the tissue to attain approximately uniform concentrations in cells and media. Whereas the slices in the glucose medium attained the same equilibrium water content as those incubated in PEG medium alone, the final water content of slices in the medium containing additional NaCl was significantly lower. This difference might have resulted from depression of intracellular colloid osmotic pressure by the high salt concentration.
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PMID:The effects of high concentrations of an electrolyte on the swelling of non-metabolizing tissue slices. 555 65

Catalase in extracts of the extreme halophile Halobacterium cutirubrum exhibits up to threefold stimulation by 0.5 to 1.5 m monovalent salts and by 0.1 m divalent salts. Above these concentrations, inhibition of enzyme activity is observed. The inhibitory effect, and to some extent the stimulation, is salt-specific; the effectiveness of a salt in inhibiting enzyme activity depends on both cation and anion. Thus, the order of effectiveness is MgCl(2) > LiCl > NaCl > KCl > NH(4)Cl, and LiCl > LiNO(3) > Li(2)SO(4). The magnitude of enzyme inhibition for the salts tested is positively correlated with their molar vapor pressure depression in aqueous solution. Stimulation of enzyme activity was observed when one salt was added at its optimal concentration in the presence of inhibiting concentrations of another salt, indicating that the effect on the enzyme is not due to changing water activity but probably to enzyme-salt interaction. Aqueous solutions of ethylene glycol, glycerol, and dimethyl sulfoxide containing no ions influence enzyme activity in the same manner as do salts.
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PMID:Effect of salts and organic solvents on the activity of Halobacterium cutirubrum catalase. 578 14

Short-term and subchronic vapor inhalation studies have shown that there are pronounced differences in the toxicological properties of ethylene glycol monomethyl ether (EGME) and propylene glycol monomethyl ether (PGME). Overexposure to EGME has resulted in adverse effects on testes, bone marrow and lymphoid tissues in laboratory animals. PGME does not affect these tissues, and instead, overexposure to PGME has been associated with increases in liver weight and central nervous system depression. EGME is primarily oxidized to methoxyacetic acid in male rats, while PGME apparently undergoes O-demethylation to form propylene glycol. Since methoxyacetic acid has been shown to have the same spectrum of toxicity as EGME in male rats, the observed differences in the toxicological properties of EGME and PGME are thought to be due to the fact that the two materials are biotransformed via different routes to different types of metabolites.
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PMID:Ethylene glycol monomethyl ether and propylene glycol monomethyl ether: metabolism, disposition, and subchronic inhalation toxicity studies. 649 8

Fifteen dogs were given 9.5 ml of ethylene glycol/kg of body weight, orally. Physical examination and clinical laboratory findings were evaluated at 1 and 3 hours after ingestion. Three of these dogs were also evaluated at 6, 9, 12, 24, 48, and 72 hours after ingestion. At 1 and 3 hours, the dogs were depressed, ataxic, and polydipsic with increased urine output and serum osmolality. Plasma bicarbonate and urine osmolality were decreased. The osmolal and anion gaps were increased at 1 and 3 hours, respectively. Calcium oxalate crystalluria was first observed at 6 hours. Diminished renal excretory function was not evident until 48 hours. Depression, ataxia, metabolic acidosis, polydipsia, and polyuria in the presence of serum hyperosmolality were early (1 and 3 hour) findings that indicated ethylene glycol intoxication in dogs.
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PMID:Early clinicopathologic findings in dogs ingesting ethylene glycol. 652 24

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

The relationship of cortisol in blood plasma with plasma calcium and phosphorus was studied from 3 days before to 2.5 days after calving in 12 dairy cows (third or more parity). Cows were in three groups: 1) paretic (displayed hypocalcemic and lateral recumbency), 2) nonparetic (plasma calcium at least 8.0 mg/100 ml), and 3) borderline (plasma calcium less than 8.0 mg/100 ml). Cortisol concentrations from 0 to 1.5 days postpartum reflected the state of calcium stress of the groups, paretic more than borderline and borderline more than nonparetic. Phosphorus was lower from 0 to 1 day postpartum in paretic cows. Calcium and phosphorus were negatively correlated (within cow) with cortisol (-.53, -.37). In experiments with goats, cortisol was released in response to hypocalcemia and displayed no activity in initiating an onset of hypocalcemia when given exogenously. Also, the observation that cortisol-treated goats responded less severely with calcium depression and recovered faster from induced hypocalcemia by ethylene glycol-bis (beta-amino-ethyl ester) N,N'-tetraacetic acid infusions suggests cortisol may aid the animal in recovering from hypocalcemia.
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PMID:Elevated plasma cortisol during induced and spontaneous hypocalcemia in ruminants. 681 10

The method by which serum osmolality is measured can significantly affect the result if certain volatiles or solvents are present in the specimen. Commonly available solvents and alcohols were added to aliquots of pooled human serum to produce toxicologically relevant concentrations. Increasing concentrations of carbon tetrachloride, chloroform, mono-n-butyl ether (butyl cellosolve), 1, 1,1 trichloroethylene, toluene, and xylene did not change vapor pressure (VP) or freezing point depression (FPD) osmolality. Acetone, ethanol, isopropanol, and methanol in increasing concentrations produced a linear increase in FPD osmolality, but no change in VP osmolality. Only ethylene glycol produced a linear increase in VP and FPD osmolality across the range of concentrations studied. Despite the excellent correlation between osmolality and ethanol concentration in prepared serum samples, this relationship could not accurately predict patient ethanol concentrations from FPD osmolality. The osmolal gap, "delta" osmolality, (measured FPD minus calculated osmolality) did not correlate with the difference between measured FPD and VP osmolalities. Patient ethanol levels could not be predicted with accuracy using an equation based on the osmolal gap or "delta" osmolality.
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PMID:Effect of alcohols and selected solvents on serum osmolality measurements. 688 6

Information from the clinical laboratory can contribute in several ways to the evaluation and management of the acute consequences of alcohol ingestion. If a blood alcohol analysis is not available, measurement of serum osmolality can be helpful. An elevated ethanol level can explain central nervous system depression. Evidence of acute or chronic alcohol use can explain atypical responses to various drugs. Severe acidosis in association with an increased anion gap may suggest ingestion of other toxic volatiles, such as methanol or ethylene glycol. Alcoholic ketoacidosis, also associated with a large anion gap, may occur in the absence of measureable alcohol or positive test for ketones.
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PMID:Acute toxicology of ethanol ingestion. Role of the clinical laboratory. 700 69


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