Medical toxicology最新文献

{"title":"Mechanisms of Cyanotoxin Toxicity—Carcinogenicity, Anticancer Potential, and Clinical Toxicology","authors":"D. Vankova, M. Pasheva, Y. Kiselova-Kaneva, Dobri Ivanov, Diana Ivanova","doi":"10.5772/INTECHOPEN.88016","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.88016","url":null,"abstract":"Cyanoprokaryotes are distributed worldwide and they produce various bioactive compounds, including cyanotoxins. The major route of human exposure to cyanotoxins is the oral intake by using contaminated drinking water, by incidental intake of contaminated water during recreational and professional activities, and by consuming contaminated food or dietary supplements prepared from cyanobacteria. The prolonged chronic exposure to low concentrations of cyanotoxins provokes cell damage and may increase the risk for cancer development. Due to the variety of cyanotoxin chemical structures, different mechanisms of their toxic effects are known. At the same time, some of the natural compounds produced by cyanoprokaryotes have anticancer potential and are promising sources for the development of novel drugs. This chapter is dedicated to the target mechanisms behind the effects of the widely distributed cyanotoxins with an impact on human health, microcystins, nodularins, and cylindrospermopsin.","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41359437","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":"Focal motor status epilepticus following treatment with azlocillin and cefotaxime.","authors":"S J Wroe, J E Ellershaw, J A Whittaker, A Richens","doi":"10.1007/BF03259866","DOIUrl":"https://doi.org/10.1007/BF03259866","url":null,"abstract":"","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"233-4"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14241508","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":"Chronic low-level lead exposure. Its role in the pathogenesis of hypertension.","authors":"D S Sharp,&nbsp;C E Becker,&nbsp;A H Smith","doi":"10.1007/BF03259865","DOIUrl":"https://doi.org/10.1007/BF03259865","url":null,"abstract":"<p><p>Lead is a common element in the earth's crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure. This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the dose-response characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation. The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular perturbations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a 'safe' level of environmental lead exposure, and whether a proportion of essential hypertension could be 'cured' by chelation therapy.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"210-32"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259865","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14427909","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":"Adverse reactions with oral and parenteral gold preparations.","authors":"E C Tozman, N L Gottlieb","doi":"10.1007/BF03259863","DOIUrl":"10.1007/BF03259863","url":null,"abstract":"<p><p>Auranofin (triethylphosphine gold), an oral gold preparation, has recently been made available, and along with injectable gold preparations, is of therapeutic value for rheumatoid arthritis. Serious gold toxicity is uncommon, and drug-related deaths rare. Many potential adverse reactions are similar, including dermatitis, stomatitis, thrombocytopenia, leucopenia, and proteinuria, generally with increased incidence in the injectable gold-treated patients. Oral gold is associated with benign lower gastrointestinal side effects, including diarrhoea, loose stools and abdominal cramps that are often dose-related and resolve spontaneously. The incidence of severe reactions such as thrombocytopenia, aplastic anaemia and exfoliative dermatitis is lower with oral gold than injectable preparations, and contributes to a superior risk-benefit ratio. The treatment of gold toxicity depends on the type and extent of organ involvement.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"177-89"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14425422","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":"Aetiology and treatment of neuroleptic malignant syndrome.","authors":"C Harpe, A Stoudemire","doi":"10.1007/BF03259862","DOIUrl":"10.1007/BF03259862","url":null,"abstract":"<p><p>The clinical triad of fever, movement disorder, and altered mentation known as NMS represents an infrequent yet highly lethal side effect of neuroleptic therapy. Although awareness and recognition are on the rise, underdiagnosis of the disorder may represent a neglected clinical problem of major proportions considering the number of patients treated with neuroleptics. The recognition of problems such as NMS and tardive dyskinesia point out the need for investigation of low-dose efficacy and neuroleptic serum levels. The idea that neuroleptics are free of severe side effects has created a clinical fallacy that high doses of high potency neuroleptics should be administered to acutely psychotic patients and that low doses of neuroleptics may be used for various diagnostic entities. The emphasis on NMS and its 20% mortality rate should point out that neuroleptics should only be used when clinically indicated to treat psychosis and should be given in the lowest possible dose that achieves antipsychotic effects. Although treatment strategies are still being formulated, aggressive medical care and specific drug therapies exist to reverse the symptoms of this syndrome. With proper education, psychiatrists and other specialists can recognize and treat NMS effectively and thus prevent its malignant outcome.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"166-76"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14425418","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":"Aspirin and Reye's syndrome. A reappraisal.","authors":"A M Glen-Bott","doi":"10.1007/BF03259861","DOIUrl":"10.1007/BF03259861","url":null,"abstract":"","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"161-5"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14425416","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":"Adverse cardiovascular effects of sulphonylurea drugs. Clinical significance.","authors":"R Huupponen","doi":"10.1007/BF03259864","DOIUrl":"10.1007/BF03259864","url":null,"abstract":"<p><p>Sulphonylureas are widely used in the treatment of diabetes mellitus. Since the publication of the University Groups Diabetes Program (UGDP) results the discussion on their possible cardiovascular side effects has been lively and sometimes even passionate. The initial UGDP findings about the adverse effects of tolbutamide on the cardiovascular system have been criticised, particularly for shortcomings in the study design. The results of other epidemiological studies of the sulphonylurea effects on cardiovascular morbidity and mortality published this far have been contradictory. This is understandable because the factors involved are very complex. Most of these studies have used tolbutamide only, and the findings cannot necessarily be directly extrapolated to other sulphonylureas. Only properly performed prospective studies may provide further information on this issue. High concentrations of several sulphonylureas may have inotropic effects on heart muscle in in vitro animal models, but human studies performed in vivo do not support the view of clinically significant inotropy for sulphonylureas. High concentrations of tolbutamide or glibenclamide (glyburide) may affect the myocardial metabolism in isolated organs, but the possible clinical significance of these findings remains unknown. Some epidemiological and experimental studies have associated oral antidiabetic treatment with the occurrence of cardiac arrhythmias or increased digitalis toxicity. Only a few results are available, and there may be differences between the sulphonylureas in this respect. Antiaggregatory properties have been postulated for some sulphonylureas. Gliclazide, in particular, has been studied, but some other compounds of this class have also been effective in short term studies. If confirmed, these effects on haemostasis would be noteworthy. The sulphonylurea effects on serum lipids, especially on HDL-cholesterol, have been discussed widely during the last few years. Decreases in HDL-cholesterol concentrations were suggested to be associated with sulphonylurea therapy. However, these findings were not confirmed in recent cross-sectional and longitudinal studies performed with different sulphonylureas. Chlorpropamide, and to a lesser extent tolbutamide, may cause dilutional hyponatraemia and aggravate existing heart failure. Glibenclamide may increase the clearance of water in the kidney.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 3","pages":"190-209"},"PeriodicalIF":0.0,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14427907","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 cholestasis.","authors":"H J Zimmerman, J H Lewis","doi":"10.1007/BF03260010","DOIUrl":"10.1007/BF03260010","url":null,"abstract":"<p><p>Intrahepatic cholestasis, defined as arrested bile flow, mimics extrahepatic obstruction in its biochemical, clinical and morphological features. It may be due to hepatocyte lesions of which there are three types, termed canalicular, hepatocanalicular and hepatocellular, respectively; or it may be due to ductal lesions at the level of the cholangiole or portal or septal ducts. Defective bile flow due to hepatic lesions reflects abnormal modification of the ductular bile. Defective formation of canalicular bile may involve bile acid-dependent or independent flow. It appears to result most importantly from defective secretion of bile acid-dependent flow secondary to defective uptake from sinusoidal blood, defective transcellular transport and defective secretion; or from regurgitation of secreted bile via leaky tight junctions. An independent defect in bile acid-independent flow is less clear. Defective flow of bile along the canaliculus may reflect increased viscosity and impaired canalicular contractility secondary to injury of the pericanalicular microfibrillar network. Impaired flow beyond the canaliculus may result from ductal injury. Sites of lesions that contribute to cholestasis include the sinusoidal and canalicular plasma membrane, the pericanalicular network and the tight junction and, less certainly, microtubules and microfilaments and Golgi apparatus. A number of drugs that lead to cholestasis have been found to lead to injury at one or more of these sites. Other agents (alpha-naphthylisothiocyanate, methylenedianiline, contaminated rapeseed oil, paraquat) lead to ductal injury resulting in cholestasis. Reports of inspissated casts in ductules (benoxaprofen jaundice) and injury to the major excretory tree (5-fluorouridine after hepatic artery infusion) have led to other forms of ductal cholestasis. Most instances of drug-induced cholestasis present as acute, transient illness, although important chronic forms also occur. The clinical features include the reflection of the cholestasis (pruritus, jaundice), systemic manifestations and extrahepatic organ involvement. While nearly all classes of medicinal agents include some that can lead to cholestasis, there are differences among the various categories. Phenothiazines and related antipsychotic and 'tranquillizer' drugs characteristically lead to cholestatic hepatic injury. The tricyclic antidepressants may lead to cholestatic or hepatocellular injury.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 2","pages":"112-60"},"PeriodicalIF":0.0,"publicationDate":"1987-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14675648","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 acetylcysteine in clinical toxicology.","authors":"R J Flanagan","doi":"10.1007/BF03260008","DOIUrl":"10.1007/BF03260008","url":null,"abstract":"","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 2","pages":"93-104"},"PeriodicalIF":0.0,"publicationDate":"1987-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14695427","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 naltrexone in the management of drug abuse.","authors":"H M Ginzburg, M G MacDonald","doi":"10.1007/BF03260007","DOIUrl":"10.1007/BF03260007","url":null,"abstract":"","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 2","pages":"83-92"},"PeriodicalIF":0.0,"publicationDate":"1987-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14675645","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}