Toxicological reviews最新文献

{"title":"Symposium on γ-Hydroxybutyrate (GHB)","authors":"J. Brent","doi":"10.2165/00139709-200423010-00001","DOIUrl":"https://doi.org/10.2165/00139709-200423010-00001","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2012-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423010-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68154868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hair in Toxicology: an Important Bio-Monitor Edited by Desmond J. Tobin","authors":"T. Sheehan","doi":"10.2165/00139709-200625010-00005","DOIUrl":"https://doi.org/10.2165/00139709-200625010-00005","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"70 1","pages":"71"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625010-00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68154990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organophosphate-induced intermediate syndrome: aetiology and relationships with myopathy.","authors":"Lakshman Karalliedde,&nbsp;David Baker,&nbsp;Timothy C Marrs","doi":"10.2165/00139709-200625010-00001","DOIUrl":"https://doi.org/10.2165/00139709-200625010-00001","url":null,"abstract":"<p><p>The intermediate syndrome (IMS) following organophosphorus (OP) insecticide poisoning was first described in the mid-1980s. The syndrome described comprised characteristic symptoms and signs occurring after apparent recovery from the acute cholinergic syndrome. As the syndrome occurred after the acute cholinergic syndrome but before organophosphate-induced delayed polyneuropathy, the syndrome was called 'intermediate syndrome'. The IMS occurs in approximately 20% of patients following oral exposure to OP pesticides, with no clear association between the particular OP pesticide involved and the development of the syndrome. It usually becomes established 2-4 days after exposure when the symptoms and signs of the acute cholinergic syndrome (e.g. muscle fasciculations, muscarinic signs) are no longer obvious. The characteristic features of the IMS are weakness of the muscles of respiration (diaphragm, intercostal muscles and accessory muscles including neck muscles) and of proximal limb muscles. Accompanying features often include weakness of muscles innervated by some cranial nerves. It is now emerging that the degree and extent of muscle weakness may vary following the onset of the IMS. Thus, some patients may only have weakness of neck muscles whilst others may have weakness of neck muscles and proximal limb muscles. These patients may not require ventilatory care but close observation and monitoring of respiratory function is mandatory. Management is essentially that of rapidly developing respiratory distress and respiratory failure. Delays in instituting ventilatory care will result in death. Initiation of ventilatory care and maintenance of ventilatory care often requires minimal doses of non-depolarising muscle relaxants. The use of depolarising muscle relaxants such as suxamethonium is contraindicated in OP poisoning. The duration of ventilatory care required by patients may differ considerably and it is usual for patients to need ventilatory support for 7-15 days and even up to 21 days. Weaning from ventilatory care is best carried out in stages, with provision of continuous positive airway pressure prior to complete weaning. Continuous and close monitoring of respiratory function (arterial oxygen saturation, partial pressure of oxygen in arterial blood, partial pressure of carbon dioxide in arterial blood) and acid-base status are an absolute necessity. Prophylactic antibiotics are usually not required unless there has been evidence of aspiration of material into the lungs. Close monitoring of fluid and electrolyte balance is mandatory in view of the profuse offensive diarrhoea that most patients develop. Maintenance of nutrition, physiotherapy, prevention of bed sores and other routine measures to minimise discomfort during ventilatory care are necessary. Recovery from the intermediate syndrome is normally complete and without any sequelae. The usefulness of oximes during the IMS remains uncertain. In animal experiments, very early a","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 1","pages":"1-14"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625010-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26155553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Veratrum poisoning.","authors":"Leo J Schep,&nbsp;David M Schmierer,&nbsp;John S Fountain","doi":"10.2165/00139709-200625020-00001","DOIUrl":"https://doi.org/10.2165/00139709-200625020-00001","url":null,"abstract":"<p><p>Several species of the Veratrum genus are associated with toxicity in humans and animals. The principal toxins are steroid alkaloids; some have a modified steroid template, whereas others differ in their esterified acid moieties. These alkaloids act by increasing the permeability of the sodium channels of nerve cells, causing them to fire continuously. Increased stimulation, associated with the vagal nerve results in a reflex that causes the triad of responses known as the Bezold-Jarisch reflex: hypotension, bradycardia and apnoea. Clinically, various Veratrum extracts were marketed for clinical use as antihypertensive drugs, but because of their narrow therapeutic index were withdrawn from the market. Following the ingestion of Veratrum alkaloids, expected signs and symptoms include vomiting and abdominal pain, followed by cardiovascular effects such as bradycardia, hypotension and cardiac conduction abnormalities and death. Similar symptoms arise in other mammalian species ingesting these alkaloids; teratogenic effects may occur to the fetuses of animals that have grazed on Veratrum californicum. Treatment consists of supportive care, with an emphasis on haemodynamic stability with fluid replacement, atropine and vasopressors. The onset of symptoms occurs between 30 minutes and 4 hours, and the duration of the illness can range from 1 to 10 days; however, with prompt supportive care, patients typically make a full recovery within 24 hours.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 2","pages":"73-8"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625020-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26242104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid rescue resuscitation from local anaesthetic cardiac toxicity.","authors":"Guy Weinberg","doi":"10.2165/00139709-200625030-00001","DOIUrl":"https://doi.org/10.2165/00139709-200625030-00001","url":null,"abstract":"<p><p>Systemic local anaesthetic toxicity is a rare but potentially fatal complication of regional anaesthesia. This toxicity is due to inhibition of ionotropic and metabotropic cell signal systems and possibly mitochondrial metabolism. It is associated with CNS excitation and, in the extreme, refractory cardiac dysfunction and circulatory collapse. Infusion of lipid emulsion has been shown in animal models to reliably reverse otherwise intractable cardiac toxicity and the mechanism of lipid rescue is probably a combination of reduced tissue binding by re-established equilibrium in a plasma lipid phase and a beneficial energetic-metabolic effect. Recent case reports have suggested the clinical efficacy of lipid infusion by the recovery of patients from intractable cardiac arrest. Future areas of investigation will focus on improved treatment regimes and better understanding of the mechanism of lipid rescue, which might allow superior alternative therapies, or treatment of other toxic events. An educational website has been established to help disseminate information about lipid emulsion therapy and to serve as a medium for physicians to share experiences or thoughts on the method and local anaesthetic toxicity.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 3","pages":"139-45"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625030-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26463689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diacetyl-induced lung disease.","authors":"Philip Harber,&nbsp;Kaochoy Saechao,&nbsp;Catherine Boomus","doi":"10.2165/00139709-200625040-00006","DOIUrl":"https://doi.org/10.2165/00139709-200625040-00006","url":null,"abstract":"<p><p>Diacetyl is a diketone flavouring agent that is commonly employed for buttery taste as well as other purposes. Industrial exposure to flavouring agents, particularly diacetyl, has recently been associated with bronchiolitis obliterans, a severe respiratory illness producing fibrosis and obstruction of the small airways. This has been most commonly reported in the microwave popcorn production industry, but it has occurred elsewhere. In addition to bronchiolitis obliterans, spirometry abnormalities (fixed airflow obstruction) and respiratory symptoms have been associated with exposure. A direct effect on the respiratory epithelium with the disorganised fibrotic repair appears most likely as the underlying mechanism. Current data suggest that diacetyl is the agent responsible, although it is possible that diacetyl is simply a marker for another causative agent.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 4","pages":"261-72"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625040-00006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26543370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic drug monitoring of digoxin: impact of endogenous and exogenous digoxin-like immunoreactive substances.","authors":"Amitava Dasgupta","doi":"10.2165/00139709-200625040-00007","DOIUrl":"https://doi.org/10.2165/00139709-200625040-00007","url":null,"abstract":"<p><p>Digoxin is a cardioactive drug with a narrow therapeutic range. Therapeutic drug monitoring is essential in clinical practice for efficacy as well as to avoid digoxin toxicity. Immunoassays are commonly used in clinical laboratories for determination of serum or plasma digoxin concentrations. Unfortunately, digoxin immunoassays are affected by both endogenous and exogenous compounds. Endogenous compounds are termed 'digoxin-like immunoreactive substances' (DLIS), which are found in elevated concentrations in volume-expanded patients. Exogenous compounds that interfere with digoxin assays are various drugs such as spironolactone, potassium canrenoate as well as Digibind (Fab fragment of antidigoxin antibody), which is used in treating life-threatening digoxin overdose. Moreover, various Chinese medicines such as Chan Su, Lu-Shen Wan and oleander-containing herbal preparations also interfere with serum digoxin measurements by immunoassays. Monitoring unbound (free) digoxin concentration may under certain circumstances eliminate such interferences. Clinicians should be aware of limitations of therapeutic drug monitoring of digoxin using immunoassays.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 4","pages":"273-81"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625040-00007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26542838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The value of morphological neuroimaging after acute exposure to toxic substances.","authors":"Philippe Hantson,&nbsp;Thierry Duprez","doi":"10.2165/00139709-200625020-00003","DOIUrl":"https://doi.org/10.2165/00139709-200625020-00003","url":null,"abstract":"<p><p>Many toxic agents induce brain dysfunction and/or lesions. Modern neuroimaging techniques, such as CT and more recently magnetic resonance imaging (MRI), are able to demonstrate toxic brain lesions at both early and delayed phases of disease progression. In the early phase, neuroimaging enables the detection of acutely injured brain areas responsible for sudden onset of neurological dysfunction, but the severity and the extension of brain lesions on neuroimages do not necessarily parallel the severity of the clinical status. In the chronic phase, when neurological dysfunction has become permanent, neuroimaging allows precise identification of neuroanatomical sequelae that do not necessarily match the severity of the chronic neurological impairment. Papers in the medical imaging literature have dealt mainly with the brain changes induced by 'chronic exposure' to toxic substances such as solvents or heavy metals. This article selectively reviews the main radiological changes observed on CT/magnetic resonance (MR) neuroimages after 'acute exposure' to industrial products (methanol [methyl alcohol], ethylene glycol), environmental agents (cyanide, carbon monoxide), pharmaceuticals (insulin, valproic acid) and illicit substances (heroin, cocaine). Different kinds of lesions, which lack specificity for toxic injury, can be observed on radiological images, but deep grey matter lesions with symmetrical distribution throughout basal ganglia are most often seen. However, such findings have also been reported after anoxic-ischaemic insults or during severe metabolic disturbances. Lesions in the white matter may also be present in the case of acute exposure to toxic agents. The true prognostic value of toxic-induced brain changes in the acute phase in CT or MR studies is unclear, although serial MRI may add new information as may quantitative or molecular imaging techniques such as the MR diffusion-weighted imaging or MR spectroscopy.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 2","pages":"87-98"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625020-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26242106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manganese: pharmacokinetics and molecular mechanisms of brain uptake.","authors":"Michael Aschner,&nbsp;David C Dorman","doi":"10.2165/00139709-200625030-00002","DOIUrl":"https://doi.org/10.2165/00139709-200625030-00002","url":null,"abstract":"<p><p>Manganese is an essential mineral that is found at low levels in virtually all diets. Manganese ingestion represents the principal route of human exposure, although inhalation also occurs, predominantly in occupational cohorts. Regardless of intake, animals generally maintain stable tissue manganese levels as a result of homeostatic mechanisms that tightly regulate the absorption and excretion of this metal. However, high-dose exposures are associated with increased tissue manganese levels, causing adverse neurological, reproductive and respiratory effects. In humans, manganese-induced neurotoxicity is associated with a motor dysfunction syndrome, commonly referred to as manganism or Parkinsonism, which is of paramount concern and is considered to be one of the most sensitive endpoints. This article focuses on the dosimetry of manganese with special focus on transport mechanisms of manganese into the CNS. It is not intended to be an exhaustive review of the manganese literature; rather it aims to provide a useful synopsis of contemporary studies from which the reader may progress to other research citations as desired. Specific emphasis is directed towards recent published literature on manganese transporters' systemic distribution of manganese upon inhalation exposure as well as the utility of magnetic resonance imaging in quantifying brain manganese distribution.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 3","pages":"147-54"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625030-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26463690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium fluoroacetate poisoning.","authors":"Alex T Proudfoot,&nbsp;Sally M Bradberry,&nbsp;J Allister Vale","doi":"10.2165/00139709-200625040-00002","DOIUrl":"https://doi.org/10.2165/00139709-200625040-00002","url":null,"abstract":"<p><p>Sodium fluoroacetate was introduced as a rodenticide in the US in 1946. However, its considerable efficacy against target species is offset by comparable toxicity to other mammals and, to a lesser extent, birds and its use as a general rodenticide was therefore severely curtailed by 1990. Currently, sodium fluoroacetate is licensed in the US for use against coyotes, which prey on sheep and goats, and in Australia and New Zealand to kill unwanted introduced species. The extreme toxicity of fluoroacetate to mammals and insects stems from its similarity to acetate, which has a pivotal role in cellular metabolism. Fluoroacetate combines with coenzyme A (CoA-SH) to form fluoroacetyl CoA, which can substitute for acetyl CoA in the tricarboxylic acid cycle and reacts with citrate synthase to produce fluorocitrate, a metabolite of which then binds very tightly to aconitase, thereby halting the cycle. Many of the features of fluoroacetate poisoning are, therefore, largely direct and indirect consequences of impaired oxidative metabolism. Energy production is reduced and intermediates of the tricarboxylic acid cycle subsequent to citrate are depleted. Among these is oxoglutarate, a precursor of glutamate, which is not only an excitatory neurotransmitter in the CNS but is also required for efficient removal of ammonia via the urea cycle. Increased ammonia concentrations may contribute to the incidence of seizures. Glutamate is also required for glutamine synthesis and glutamine depletion has been observed in the brain of fluoroacetate-poisoned rodents. Reduced cellular oxidative metabolism contributes to a lactic acidosis. Inability to oxidise fatty acids via the tricarboxylic acid cycle leads to ketone body accumulation and worsening acidosis. Adenosine triphosphate (ATP) depletion results in inhibition of high energy-consuming reactions such as gluconeogenesis. Fluoroacetate poisoning is associated with citrate accumulation in several tissues, including the brain. Fluoride liberated from fluoroacetate, citrate and fluorocitrate are calcium chelators and there are both animal and clinical data to support hypocalcaemia as a mechanism of fluoroacetate toxicity. However, the available evidence suggests the fluoride component does not contribute. Acute poisoning with sodium fluoroacetate is uncommon. Ingestion is the major route by which poisoning occurs. Nausea, vomiting and abdominal pain are common within 1 hour of ingestion. Sweating, apprehension, confusion and agitation follow. Both supraventricular and ventricular arrhythmias have been reported and nonspecific ST- and T-wave changes are common, the QTc may be prolonged and hypotension may develop. Seizures are the main neurological feature. Coma may persist for several days. Although several possible antidotes have been investigated, they are of unproven value in humans. The immediate, and probably only, management of fluoroacetate poisoning is therefore supportive, including the correction of hyp","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 4","pages":"213-9"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625040-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26543366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}