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 total of 23 men complained of neurological symptoms after a single severe exposure to toluene di-isocyanate. Effects of exposure were immediate in five men and consisted of euphoria, ataxia, and loss of consciousness. These men and nine others complained of headache, difficulty in concentration, poor memory, and confusion during the next three weeks. Four years later it was found that nine further men had experienced symptoms that they had not been aware of at three weeks. In all, 13 men still complained of poor memory, personality change, irritability, or depression after four years. Psychometric testing showed a selective defect for relatively long-term recall in those with persistent symptoms at four years.
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PMID:Neurological complications after a single severe exposure to toluene di-isocyanate. 17 62

A 38-year-old male developed acute oliguric renal failure following repeated glue sniffing for about 8 hours. In addition, he had severe liver cell injury, mild myonecrosis and bone marrow depression indicating generalized tissue toxicity. The high urinary spot sodium during the oliguric phase and the total renal functional recovery after a period of oliguria followed by polyuria favoured a diagnosis of acute toxic tubular necrosis causing acute renal failure. Toluene which is used as the solvent is presumably the toxic agent involved in glue sniffing. It is advised that toluene inhalation be considered in the differential diagnosis of acute renal failure especially in the young. Literature on the renal toxicity of toluene is briefly reviewed.
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PMID:Oliguric acute renal failure due to glue-sniffing. Case report. 194 58

Groups of 50 F344/N rats of each sex and 50 B6C3F1 mice of each sex were gavaged with corn oil or a mixture of toluene diisocyanate (TDI) in corn oil for 5 days per week for 105 or 106 weeks. Female rats and mice were given doses of 60 or 120 mg/kg body weight, while male rats received 30 or 60 mg/kg, and male mice received 120 or 240 mg/kg. The TDI reacted with the moisture in the corn oil vehicle resulting in doses that were 10% to 23% below the target dose concentrations. The chemical product used was commercial grade TDI, which was an 80%-20% mixture of the 2,4- and 2,6-isomers. Chemical disposition and metabolism studies were conducted with each of the radiolabelled TDI isomers in male rats. Absorption of both of the TDI isomers occurred, with the highest concentrations found in the stomach, cecum, large intestine, and bladder. Excretion occurred via the feces and urine. The major metabolic products from the metabolism of 2,4-TDI were shown to be identical with those from the metabolism of the carcinogen, 2,4-diaminotoluene, whereas the metabolism of the 2,6-TDI isomer yielded one major product, identified as 2,6-bis(acetylamino)toluene. Greater than 10% depression in body weight gain occurred in all dosed groups of rats throughout most of the study. The major non-neoplastic lesions that were observed in both sexes of the TDI-exposed rats were dose-related increases in acute broncho-pneumonia, characterized as chemical pneumonitis, with incidences as high as 50%. In mice mean body weight gain was depressed in dosed male and in high dose females. The principle non-neoplastic lesion in mice that was attributed to chemical treatment was cytomegaly of the kidney tubular epithelium in males. Survival in all groups of dosed rats was significantly lower than in controls. A dose-dependent pattern of mortality did not commence until 70 weeks of exposure, demonstrating that toluene diisocyanate elicited a cumulative toxic response. There was also significantly lower survival in high dose male, but not female mice, by comparison to controls. Despite the reduction of power and sensitivity in the rat studies caused by early mortality, statistically significant increases in tumor incidences were observed in many different target organs. TDI was carcinogenic in F344/N rats, causing subcutaneous fibromas and fibrosarcomas in males and females, pancreatic acinar cell adenomas in males, and pancreatic islet cell adenomas, neoplastic nodules of the liver, and mammary gland tumors in females.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The carcinogenic activity of commercial grade toluene diisocyanate in rats and mice in relation to the metabolism of the 2,4- and 2,6-TDI isomers. 166 67

Acute poisoning with organic solvents and other volatile compounds now usually follows deliberate inhalation (volatile substance abuse) or ingestion of these compounds. Solvents from adhesives, typewriter correction and dry cleaning fluids, cigarette lighter refills (butane) and aerosol propellants are commonly abused. The major risk is that of sudden death. Arrhythmias leading to cardiac arrest are thought to cause most deaths, but anoxia, respiratory depression and vagal stimulation leading to cardiac arrest may also contribute, as may indirect causes such as aspiration of vomit or trauma. In the United Kingdom (UK), 3.5 to 10% of young people have at least experimented with volatile substance abuse and mortality is more than 100 per annum. The products abused are cheap and readily available despite legislation designed to limit supply. Volatile substance abuse is not illegal and only a minority of abusers are known to progress to heavy alcohol or illicit drug use. Prevention of abuse by education, not only of children but also of parents, teachers, retailers and health care workers, is important in limiting the problem. However, volatile substance abuse-related deaths are still increasing in the UK despite many measures aimed at prevention. Clinically, volatile substance abuse is characterised by a rapid onset of intoxication and rapid recovery. Euphoria and disinhibition may be followed by hallucinations, tinnitus, ataxia, confusion, nausea and vomiting. It is important not to further alarm the patient if signs of serious toxicity are present, since a cardiac arrest may be precipitated. Further exposure should be prevented and the patient resuscitated and given supplemental oxygen if necessary. Cardiac arrhythmias should be treated conventionally and respiratory failure managed supportively. Long term exposure to n-hexane is associated with the development of peripheral neuropathy, while prolonged abuse (notably of toluene or chlorinated solvents) can cause permanent damage to the central nervous system, heart, liver, kidney and lungs. Knowledge of the routes of absorption, distribution and excretion of volatile compounds, and of the rates governing these processes, is important in understanding the rate of onset, intensity and duration of intoxication, and rate of recovery after volatile substance abuse. In addition, such knowledge is helpful when the clinician is attempting to interpret the results of toxicological analyses performed on samples (blood, other tissues, urine) from such patients. Many volatile substances are partly metabolised, the metabolites being eliminated in exhaled air or in urine. Although metabolism normally results in detoxification, enhanced toxicity may also result as with carbon tetrachloride, chloroform, dichloromethane, n-hexane, trichloroethylene and possibly halothane.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An introduction to the clinical toxicology of volatile substances. 222 69

The metabolite S-adenosyl-L-methionine (SAMe), when prepared as the stable p-toluene-sulfonate complex of its sulfate salt and given parenterally in high doses, appears to have mood-elevating effects in depressed adults. The material is remarkably well tolerated when given by injection or intravenous infusion for this purpose, even in elderly or demented patients. Assuming that the toluene sulfonate component is inert, SAMe appears to have central neuropharmacologic effects after systemic injection in high doses. Nevertheless, the functional consequences of these remain unclear and, indeed, the ability of exogenous SAMe to reach the brain, and especially neuronal cytoplasm, is limited. SAMe has small effects on monoamine metabolism and, after injection, appears to have effects on the microviscosity of cell membranes that may be related to stimulation of phospholipid synthesis. The recent introduction of an orally administered form of SAMe for use in the treatment of osteoarthritis promises to stimulate further study of SAMe in disease-associated depression, major depressive disorder, and other neuropsychiatric conditions.
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PMID:Neuropharmacology of S-adenosyl-L-methionine. 331 48

Long-Evans hooded rats were exposed to single doses of toluene (PO) at 0, 250, 500 and 1000 mg/kg, to p-xylene (PO) at 0, 125, 250, 500, 1000 and 2000 mg/kg, and to inhalation of p-xylene for 4 hr at 0, 800 or 1600 ppm. The functional integrity of the visual system was evaluated using flash-evoked potentials (FEPs). The data indicated a significant depression in amplitude of FEP peak N3 at 250 mg/kg and higher dosages of toluene and p-xylene. A similar depression in peak N3 amplitude was observed following inhalation exposure to 1600 ppm p-xylene. The effects produced by oral administration of 500 mg/kg p-xylene or toluene lasted at least 8 hr, while the effect of inhaled p-xylene dissipated within 75 min of removal from the exposure. FEP peak N3 is presumed to be related to arousal, such that increases in arousal from a relaxed state should decrease amplitude. Rats administered amphetamine in dosages of 0.6, 1.2 and 2.5 mg/kg (known to increase arousal) also had reduced N3 amplitude. The effects of p-xylene and toluene on FEPs, while indicative of altered processing of visual information, may be secondary to changes in arousal or excitability.
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PMID:Acute exposures to p-xylene and toluene alter visual information processing. 339 23

Effects of experimental exposure to toluene (3.2 mmol/m3, ie, 300 mg/m3) for 4.5 h and ethanol ingestion (15 mmol/kg) on the results of four performance tests, symptoms, mood, and physiological indices of wakefulness were studied in 12 male volunteers. Toluene exposure produced symptoms like headache and local irritation, as well as a weak depression of heart rate during rest, but did not reduce performance capability. Ethanol ingestion impaired performance on two of the tests and also increased heart rate. Mood was likewise altered by ethanol, but no increase in subjective symptoms due to ethanol ingestion could be demonstrated. Physiological indices of wakefulness were not affected by toluene exposure or by ethanol intake. No interaction effects were found.
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PMID:Experimental exposure to toluene in combination with ethanol intake. Psychophysiological functions. 372 94

Group motility was recorded continuously in male rats during the inhalation of benzene, toluene, ethylbenzene, o-, m- and p-xylene vapours. The solvents were applied in at least six concentrations, up to those inducing anaesthesia. Minimum narcotic concentrations (ppm) were: 5940 (benzene), 3590 (toluene), 2180 (ethyl-benzene), 2180 (0-xylene), 2100 (m-xylene), and 1940 (p-xylene). The results indicate that prenarcotic concentrations of these structurally related aromatic hydrocarbons and also the xylene isomers elicit qualitatively and quantitatively different acute behavioral effects. Except o-xylene which caused depression only the agents produced bell-shaped concentration-action curves characteristic of the biphasic effect, i.e., activation at lower and depression at higher concentrations. The curves differed in form and magnitude depending on the stimulatory potency and on the range of effective concentrations. Based on arbitrary assessment of central excitation, the five aromatics may be ranked as follows: benzene and toluene (striking activation), p-xylene (marked activation), ethylbenzene (moderate activation), m-xylene (slight activation). At the same time, high degree of motor incoordination, and in the case of benzene and p-xylene, also marked tremor could be seen.
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PMID:Changes in the rat's motor behaviour during 4-hr inhalation exposure to prenarcotic concentrations of benzene and its derivatives. 375 4

It has been proposed that concomitant substances of abuse may have additive or synergistic properties such that alcoholics using other substances of abuse concurrently may have a harder time giving up alcohol than alcoholics abusing only alcohol. The present study surveyed 291 alcoholics in an alcohol treatment program and 86 social drinker controls matched on age, education, SES and gender. Alcohol consumption, smoking, coffee intake, other substances of abuse. Beck depression and Spielberger Anxiety (State) were measured. Alcoholics drank significantly more alcohol than did social drinkers per day (350.19 cc versus 28.08 cc, p less than 0.001), consumed more caffeine/day (486.3 mg versus 339.9 mg, p less than 0.002), smoked more cigarettes/day (27.8 versus 12.8, p less than 0.001), were more depressed (16.8 versus 4.4 (Beck), p less than 0.0001), had lower internal locus of control scores (37.6 versus 39.7, p less than 0.005), had higher scores on control by chance (22.7 versus 20.2, p less than 0.03) and were significantly more anxious (52.5 versus 33.9 on Spielberger's State Inventory p less than 0.0001). Some patients used stimulants, tranquilizers, depressants, narcotics or toluene. Only 3/258 abused alcohol without using other drugs. Results support earlier studies showing strong associations between alcohol and smoking and between alcohol and caffeine consumption. The alcoholic abusing only alcohol is very rare. Treatment programs need to pay attention to concomitant drugs of abuse.
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PMID:Treatment of alcoholism and concomitant drugs of abuse. 402 79

Acute effects of a single i.p. injection of toluene on circadian rhythms of sleep-wakefulness were investigated in rats which were chronically implanted with EEG and EMG electrodes for polygraphic recordings. The toluene injection produced an initial increase in wakefulness (W) and a subsequent increase in slow-wave sleep (SWS) during the dark period. In an attempt to clarify mechanisms of these biphasic effects of toluene on sleep-wakefulness rhythms, brain monoamines and their metabolites were determined at the times of the initial increase in W and the increased SWS. The initial increase in W was associated with an increase in cortical NA, MHPG and 5-HT together with a decrease in cortical 5-hydroxyindoleacetic acid (5-HIAA), while the increased SWS during the dark period was associated with an increase in 5-HIAA and a concomitant decrease in 3-methoxy-4-hydroxyphenylglycol (MHPG). The toluene-induced changes in sleep-wakefulness seemed to be manifested at lower blood levels of toluene than the behavioral signs of central nervous system (CNS) depression. These biphasic effects of toluene on circadian sleep-wakefulness rhythms are discussed in terms of the reciprocal interactions between central 5-HT and NA neurons.
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PMID:Acute effects of toluene on circadian rhythms of sleep-wakefulness and brain monoamine metabolism in rats. 608 32


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