Toxicological reviews最新文献

{"title":"Resolving disputes about toxicological risks during military conflict : the US Gulf War experience.","authors":"Kenneth C Hyams,&nbsp;Mark Brown,&nbsp;David S White","doi":"10.2165/00139709-200524030-00009","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00009","url":null,"abstract":"<p><p>In the last 15 years, the US and UK have fought two major wars in the Persian Gulf region. Controversy has arisen over the nature and causes of health problems among military veterans of these two wars. Toxic exposures have been hypothesised to cause the majority of the long-term health problems experienced by veterans of the 1991 Gulf War. The assessment of these toxic exposures and the resolution of controversy about their health effects provide a unique case study for understanding how toxicological disputes are settled in the US. Neither clinical examination of ill war veterans nor scientific research studies have been sufficient to answer contentious questions about toxic exposures. Numerous expert review panels have also been unable to resolve these controversies except for the US National Academy of Sciences Institute of Medicine (IOM). The IOM has conducted exhaustive and independent investigations based on peer-reviewed scientific literature related to potential health risks during the two Gulf Wars. In four recent studies, IOM committees identified a wide range of previously documented illnesses associated with common occupational and environmental exposures after considering thousands of relevant publications; however, they did not identify a new medical syndrome or a specific toxic exposure that caused widespread health problems among Gulf War veterans. These IOM studies have, therefore, added little to our basic knowledge of environmental hazards because most of the health effects were well known. Nevertheless, this expert review process, which is on-going, has been generally acceptable to a wide range of competing interests because the findings of the IOM have been perceived as scientifically credible and independent, and because none of the postulated toxicological risks have been completely ruled-out as possible causes of ill health among veterans.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"167-80"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781235","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":"Hydrogen peroxide poisoning.","authors":"Barbara E Watt,&nbsp;Alex T Proudfoot,&nbsp;J Allister Vale","doi":"10.2165/00139709-200423010-00006","DOIUrl":"https://doi.org/10.2165/00139709-200423010-00006","url":null,"abstract":"<p><p>Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure ","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 1","pages":"51-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423010-00006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40895093","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":"Glyphosate poisoning.","authors":"Sally M Bradberry, Alex T Proudfoot, J Allister Vale","doi":"10.2165/00139709-200423030-00003","DOIUrl":"10.2165/00139709-200423030-00003","url":null,"abstract":"<p><p>Glyphosate is used extensively as a non-selective herbicide by both professional applicators and consumers and its use is likely to increase further as it is one of the first herbicides against which crops have been genetically modified to increase their tolerance. Commercial glyphosate-based formulations most commonly range from concentrates containing 41% or more glyphosate to 1% glyphosate formulations marketed for domestic use. They generally consist of an aqueous mixture of the isopropylamine (IPA) salt of glyphosate, a surfactant, and various minor components including anti-foaming and colour agents, biocides and inorganic ions to produce pH adjustment. The mechanisms of toxicity of glyphosate formulations are complicated. Not only is glyphosate used as five different salts but commercial formulations of it contain surfactants, which vary in nature and concentration. As a result, human poisoning with this herbicide is not with the active ingredient alone but with complex and variable mixtures. Therefore, It is difficult to separate the toxicity of glyphosate from that of the formulation as a whole or to determine the contribution of surfactants to overall toxicity. Experimental studies suggest that the toxicity of the surfactant, polyoxyethyleneamine (POEA), is greater than the toxicity of glyphosate alone and commercial formulations alone. There is insufficient evidence to conclude that glyphosate preparations containing POEA are more toxic than those containing alternative surfactants. Although surfactants probably contribute to the acute toxicity of glyphosate formulations, the weight of evidence is against surfactants potentiating the toxicity of glyphosate. Accidental ingestion of glyphosate formulations is generally associated with only mild, transient, gastrointestinal features. Most reported cases have followed the deliberate ingestion of the concentrated formulation of Roundup (The use of trade names is for product identification purposes only and does not imply endorsement.) (41% glyphosate as the IPA salt and 15% POEA). There is a reasonable correlation between the amount ingested and the likelihood of serious systemic sequelae or death. Advancing age is also associated with a less favourable prognosis. Ingestion of >85 mL of the concentrated formulation is likely to cause significant toxicity in adults. Gastrointestinal corrosive effects, with mouth, throat and epigastric pain and dysphagia are common. Renal and hepatic impairment are also frequent and usually reflect reduced organ perfusion. Respiratory distress, impaired consciousness, pulmonary oedema, infiltration on chest x-ray, shock, arrythmias, renal failure requiring haemodialysis, metabolic acidosis and hyperkalaemia may supervene in severe cases. Bradycardia and ventricular arrhythmias are often present pre-terminally. Dermal exposure to ready-to-use glyphosate formulations can cause irritation and photo-contact dermatitis has been reported occasionally; these e","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 3","pages":"159-67"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423030-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25257470","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":"Drug-induced hypersensitivity: role in drug development.","authors":"Helen V Ratajczak","doi":"10.2165/00139709-200423040-00006","DOIUrl":"https://doi.org/10.2165/00139709-200423040-00006","url":null,"abstract":"<p><p>Drug-induced hypersensitivity is an adverse reaction, characterised by damaging immune-mediated responses, initiated by medicine given at therapeutic doses for prevention, diagnosis or treatment. Immune-mediated drug hypersensitivity accounts for 6-10% of the adverse drug reactions, which rank between the fourth and sixth leading causes of death in the US. With <10% of all adverse drug reactions reported, the magnitude of the problem is significant, with estimates of costs >$US30 billion annually in the US (1995 value). In addition, the costs of not determining the potential of a drug to produce hypersensitivity in the pre-clinical phase of drug development can be substantial. It has been estimated that the pre-clinical phase and clinical phase I, phase II and phase III costs are approximately $US6 million, $US12 million, $US12 million and $US100 million per drug, respectively (1999 values). It is important that investigational drugs with the potential to produce hypersensitivity reactions be identified as early in the development process as possible. Some adverse reactions to drugs can be avoided if drug-drug interactions are known or if there is a structure-activity relationship established. However, these methods are inadequate. Appropriate animal models of drug-induced hypersensitivity are needed, especially because hypersensitivity has been cited as the leading reason for taking drugs off the market. It is of critical importance to be able to predict hypersensitivity reactions to drugs. Most anaphylactic reactions occur in atopic individuals. Similarly, patients who have experienced other hypersensitivity reactions are more likely to have recurrent reactions. Therefore, animal models should be considered that predispose the animal to the reaction, such as the use of appropriate adjuvants and species. Using known positive controls of varying strengths, the investigator can rank the reaction against the positive controls as standards. This approach might yield greater results in a shorter period of time than using novel models. For the greatest safety, use of well understood models that have been thoroughly validated is imperative.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 4","pages":"265-80"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423040-00006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25114529","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":"Glaucopsia: an occupational ophthalmic hazard.","authors":"Bryan Ballantyne","doi":"10.2165/00139709-200423020-00003","DOIUrl":"https://doi.org/10.2165/00139709-200423020-00003","url":null,"abstract":"<p><p>Glaucopsia is a transient disturbance of vision that results from the development of corneal epithelial oedema and associated microcysts produced by exposure to the vapour of certain industrial chemicals, notably aliphatic, alicyclic and heterocyclic amines. After a latent period of a few hours of exposure, there is typically a blurring of vision, objects take on a blue-grey appearance and halos develop around bright objects. Corneal changes can be seen on biomicroscopy and corneal thickness increase is measurable by pachymetry. At concentrations higher than threshold values, visual acuity may be decreased, but contrast sensitivity is a better measure of visual effects. On vacating the causative vapour, vision returns to normal in a few hours without leaving permanent ocular sequelae. Vapour concentration of the causative amine is a major factor in the development of glaucopsia, and a concentration-effect relationship is usually evident. A correlation exists between the vapour concentration, degree of corneal oedema, corneal thickness and subjective symptoms, which permits no-effect and threshold-effect concentrations to be determined. The disturbance of vision is a nuisance factor and this may impair work efficiency, predispose to physical accidents and hinder the performance of coordinated tasks (e.g. driving). As a consequence, development of glaucopsia is considered a hazard and is thus an important consideration in assessing workplace safety. From a knowledge of threshold and no-effect concentrations, a workplace permissible vapour exposure concentration can be developed along with industrial hygiene precautionary measures.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 2","pages":"83-90"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423020-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24844131","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 role of diazepam in the treatment of nerve agent poisoning in a civilian population.","authors":"Timothy C Marrs","doi":"10.2165/00139709-200423030-00002","DOIUrl":"https://doi.org/10.2165/00139709-200423030-00002","url":null,"abstract":"<p><p>The main site of action of diazepam, as with other benzodiazepines, is at the GABA(A) receptor, although it has been suggested that some of the potentially beneficial actions of diazepam in nerve agent poisoning are mediated through other means. It is likely that convulsions may have long-term sequelae in the central nervous system, because of damage by anoxia and/or excitotoxicity. Numerous pharmacodynamic studies of the action of diazepam in animals experimentally poisoned with nerve agents have been undertaken. In nearly all of these, diazepam has been studied in combination with other antidotes, such as atropine and/or pyridinium oximes, sometimes in combination with pyridostigmine pretreatment. These studies show that diazepam is an efficacious anticonvulsant in nerve agent poisoning. There is considerable experimental evidence to support the hypothesis that diazepam (and other anticonvulsants) may prevent structural damage to the central nervous system as evidenced by neuropathological changes such as neuronal necrosis at autopsy. In instances of nerve agent poisoning during terrorist use in Japan, diazepam seems to have been an effective anticonvulsant. Consequently, the use of diazepam is an important part of the treatment regimen of nerve agent poisoning, the aim being to prevent convulsions or reduce their duration. Diazepam should be given to patients poisoned with nerve agents whenever convulsions or muscle fasciculation are present. In severe poisoning, diazepam administration should be considered even before these complications occur. Diazepam is also useful as an anxiolytic in those exposed to nerve agents.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 3","pages":"145-57"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423030-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25257468","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":"Toxicological and immunological aspects of occupational latex allergy.","authors":"Syed M Ahmed,&nbsp;Tar-Ching Aw,&nbsp;Anil Adisesh","doi":"10.2165/00139709-200423020-00005","DOIUrl":"https://doi.org/10.2165/00139709-200423020-00005","url":null,"abstract":"<p><p>Latex allergy continues to be an important occupational health problem as latex products are used increasingly worldwide, particularly in healthcare. Although there are few epidemiological studies on the incidence of latex allergy, there has been an increase in the number of case reports over the last 10 years and, based on skin-prick tests, estimates of prevalence of latex allergy in healthcare workers range from 2% to 17%. The allergic health effects arise either from the latex proteins, generally causing a type I immediate hypersensitivity reaction, or from the chemicals added to latex during processing, causing a type IV delayed hypersensitivity reaction. Clinical manifestations of latex allergy depend on the route of exposure and occur by direct contact either with skin or mucosa, or by inhalation. The diagnosis of latex allergy is based on the history, skin tests, serological tests and challenge tests. Thirteen latex allergens have been identified and isolated so far from natural rubber latex. They differ in their potential to elicit immunological responses in individuals allergic to latex and thus have been designated as major or minor allergens. In latex gloves, cornstarch powder used as a donning agent carries latex proteins, thereby increasing inhalational and mucosal exposure to latex proteins. There also appears to be a positive correlation between protein content and allergenicity of gloves. The use of powder-free, low-protein gloves is effective in reducing symptoms and markers of sensitisation. Alternatives to latex gloves, such as nitrile or vinyl gloves are available but may be inferior in respect to manual dexterity and biological impermeability.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 2","pages":"123-34"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423020-00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24844133","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":"Poisoning due to chlorophenoxy herbicides.","authors":"Sally M Bradberry,&nbsp;Alex T Proudfoot,&nbsp;J Allister Vale","doi":"10.2165/00139709-200423020-00001","DOIUrl":"https://doi.org/10.2165/00139709-200423020-00001","url":null,"abstract":"<p><p>Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 2","pages":"65-73"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423020-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24844129","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":"Gamma-hydroxybutyrate: bridging the clinical-analytical gap.","authors":"Cynthia L Morris-Kukoski","doi":"10.2165/00139709-200423010-00004","DOIUrl":"https://doi.org/10.2165/00139709-200423010-00004","url":null,"abstract":"<p><p>Laboratory detection of gamma-hydroxybutyrate (GHB) has been published as early as the 1960s. However, wide-scale use of GHB during the 1990s has led to the development of current analytic methods to test for GHB and related compounds. Detection of GHB and related compounds can be clinically useful in confirming the cause of coma in an overdose patient, determining its potential role in a postmortem victim, as well as evaluating its use in a drug-facilitated sexual assault victim. Analytical method sensitivity must be known in order to determine the usefulness and clinical application. Most laboratory cut-off levels are based on instrument sensitivity and will not establish endogenous versus exogenous GHB levels. Interpretation of GHB levels must include a knowledge base of endogenous GHB, metabolism of GHB and related compounds, as well as postmortem generation. Due to potential analytical limitations in various GHB methods, it is clinically relevant to specifically request for GHB as well as related GHB compounds if they are also in question. Various storage conditions (collection time, types of containers, use of preservatives, storage temperature) can also affect the analysis and interpretation of GHB and related compounds.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 1","pages":"33-43"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423010-00004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40895091","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":"Oxidant stress and haemolysis of the human erythrocyte.","authors":"Marco L A Sivilotti","doi":"10.2165/00139709-200423030-00004","DOIUrl":"https://doi.org/10.2165/00139709-200423030-00004","url":null,"abstract":"<p><p>The erythrocyte is a highly specialised cell with a limited metabolic repertoire. As an oxygen shuttle, it must continue to perform this essential task while exposed to a wide range of environments on each vascular circuit, and to a variety of xenobiotics across its lifetime. During this time, it must continuously ward off oxidant stress on the haeme iron, the globin chain and on other essential cellular molecules. Haemolysis, the acceleration of the normal turnover of senescent erythrocytes, follows severe and irreversible oxidant injury. A detailed understanding of the molecular mechanisms underlying oxidant injury and its reversal, and of the clinical and laboratory features of haemolysis is important to the medical toxicologist. This review will also briefly review glucose-6-phosphate deficiency, a common but heterogeneous range of enzyme-deficient states, which impairs the ability of the erythrocyte to respond to oxidant injury.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"23 3","pages":"169-88"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200423030-00004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25257471","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}