DOCSLIB.ORG

Measurement of Enzymes in Environmental Intoxications

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Measurement of Enzymes in Environmental Intoxications ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 7, No. 3 Copyright © 1977, Institute for Clinical Science Measurement of Enzymes in Environmental Intoxications MICHAEL M. LUBRAN, M.D., Ph.D. U.C.L.A. School of Medicine, Department of Pathology, Harbor General Hospital Campus, Torrance, CA 90509 ABSTRACT The paper details the enzymes which have been shown to be affected by certain zenobiotics, principally industrial pollutants, toxic metals, toxic gases and food additives. The role of mixed function oxidases is discussed and methods of assessing their activity indicated. One of the consequences of our indus­ been investigated experimentally in trial civilization has been the creation of a animals. Data obtained from humans dangerous environment for mankind. In­ have resulted mainly from accidental or dustrial wastes pollute the atmosphere occupational exposure to relatively high and find their way into our drinking wa­ concentrations, or prolonged exposure to ter; large-scale treatment of agricultural lower concentrations, of the chemicals. areas with herbicides and pesticides Few planned experiments have been creates health hazards for farm workers carried out. Damage to the liver, kidneys, and consumers of farm products; insec­ lungs, nervous system or other target or­ ticides may persist in the environment gans is usually easily detected; conven­ and be consumed by humans; photo­ tional laboratory tests, e.g., liver function chemical smog and motor-car exhaust tests, are adequate for their investigation. fumes contain toxic materials; toxic met­ However, chronic exposure to low con­ als, such as lead, mercury and manganese centrations of xenobiotics may not pro­ are released into the environment; food duce overt effects in man but may yet be additives, coloring materials and preser­ harmful, for example, by increasing the vatives may be hazardous. Nature, un­ risk of cancer (food additives) or aided by man, is responsible for some pulmonary and cardiovascular disease environmental hazards, such as ionizing (ozone, oxides of nitrogen, carbon radiation, local concentrations of radioac­ monoxide). tive isotopes, high concentrations of fluo­ Xenobiotics or their metabolites may rides and other toxic chemicals in rivers, accumulate in the body without produc­ as well as the sunshine necessary for ing detectable effects until a critical level smog production. is reached. It thus becomes important to Foreign substances found in the envi­ distinguish between body burden and ronment are called xenobiotics. This toxic concentrations of the chemicals. word has gained acceptance, although it Because of the wide differences in the really means ‘foreign living things’ and responses of experimental animals to more correctly describes extraterrestrial xenobiotics, it is unwise to extrapolate life forms. The toxicity of xenobiotics has from animal experiments to man, except in 210 MEASUREMENT OF ENZYMES IN ENVIRONMENTAL INTOXICATIONS 211 the most general terms. Information must rivative of the enzyme is rapidly hy­ be obtained directly by observation of drolyzed and the cholinesterase activity people exposed occupationally or other­ restored. Treatment is not required as the wise to xenobiotics. As enzymes are in­ patient recovers rapidly on being removed volved in the body’s responses to xenobi­ from the toxic agent. The phosphorylated otics, either in their metabolism or as a enzyme can be reactivated rapidly by consequence of their toxic action, changes treatment of the patient with certain in the activities of specific enzymes have oximes (e.g. pralidoxime chloride or been sought as indicators of toxicity. Un­ 2-PAMCL). Without treatment, the en­ fortunately, apart from enzymes associated zyme activity is restored at the rate of 1 to 2 with liver damage, there are few enzymes percent a day. specifically related to the toxic effects of Red cell AChE, being specific for individual xenobiotics. Possibly, the ones acetylcholine, is a better indicator of in­ described will be augmented by further hibition by organophosphorus pesticides study. than is serum PChE, which has a wider substrate specificity and may measure Cholinesterases non-specific esterase activity. However, a decrease in the activity of blood cholin­ These are esterases which hydrolyze esterase, whether in the red cell or in the choline esters more rapidly than other es­ serum, indicates only exposure to the pes­ ters.3, 16>20>28-37 Acetylcholinesterase ticide. There is no correlation between the (AChE), which is found in the red cell, is degree of enzyme inhibition and the clini­ most active towards acetylcholine, its nat­ cal state ofthe patient. The measured activ­ ural substrate. At least two AChE isoen­ ity depends on the analytical method used, zymes exist. Many cholinesterases (ChE) and the degree and duration of exposure of isoenzymes (11 or more) occur in serum, the worker. Treatment should be based on jointly being called pseudocholinesterase the clinical findings and the probability of (PChE). Pseudocholinesterase acts on a exposure to organophosphorus pesticides; variety of substrates, including acetyl­ laboratory investigations should be used choline. Cholinesterases are distin­ as confirmatory tests. The effect of pes­ guished from other esterases by being in­ ticides maybe heightened in subjects with hibited by 10 |U,M eserine. genetic abnormalities of ChE. Organo­ In addition, ChE are inhibited by or- phosphorus pesticides decrease the di- ganophosphorus compounds, carbamates bucaine and fluoride numbers as well as and some sulphonyl derivatives. Lipases cholinesterase activity. Some other and carboxylesterases are also inhibited by xenobiotics, e.g., ozone and oxides of ni­ these compounds, a phenomenon leading trogen, may decrease ChE activity. some investigators to infer falsely the exis­ tence of pancreatitis. Arylesterases, which can also hydrolyze choline esters, are not Enzymes and Toxic Metals inhibited by organophosphorus com­ pounds and are not included in the PChE Lead has been the most studied metal, group, although they may be active in but mercury, cadmium, and manganese some methods used for measuring PChE produce effects on enzyme activities. activity. Lead inhibits 8-aminolevulinic acid de­ Inhibition of cholinesterases is due to hydratase (ALAD), which catalyzes the the phosphorylation or carbamylation of condensation of two molecules of the active site. Phosphorylation is irre­ 8-aminolevulinic acid to porphobilino­ versible in the body, but the carbamyl de­ gen.14 Lead also inhibits ferrochelatase, 2 1 2 LUBRAN which is involved in the formation of pressed by exposure to lead, but not heme from iron and protoporphyrin. when normal blood was treated with Other enzymes concerned with heme lead.41 The diagnostic value of ALAD ac­ synthesis may also be affected. The tivity lies in its indication of lead expo­ logarithm of ALAD activity varies in­ sure; owing to its great sensitivity to lead, versely with blood lead concentration.36 it cannot be used as an index of lead in­ No inhibitory effect probably occurs at toxication. However, with the introduc­ concentrations below about 15 fig per dl, tion of methods in which inhibited and the value depending on the age of the uninhibited activities are measured, this subject.43 conclusion may be changed.14 Although there is ample evidence for Other red cell enzymes have been the inverse relationship between blood studied in subjects exposed to lead. lead concentration and ALAD activity, it Glutathione reductase activity increases is not clear that there is a strong correla­ as blood lead increases,15,33 possibly as a tion between ALAD activity and the toxic compensatory mechanism to overcome effects of lead, particularly when blood the reduction of SH groups brought about lead concentrations are not greatly ele­ by lead. Red cell glutathione decreases as vated.42,43 It may be possible that the ob­ lead increases. The activities of carbonic served inhibition by lead is an in vitro anhydrase isoenzymes B and C increase effect, as it is prevented by EDTA (which in subjects chronically exposed to low chelates lead) and is reversed in vitro by levels of lead.39 Catalase activity falls as the addition of thiol compounds such as blood lead rises.30 Recently, a new red glutathione and dithiothreitol; the en­ cell enzyme, 5'-ribonucleotide phos- zyme is strongly inhibited in vitro by the phohydrolase (E.C. 3.1.3.5) has been de­ addition of lead salts. scribed.24 It catalyzes the hydrolysis However, the toxic effects of lead in re­ of uridine - 5' - monophosphate and lation to ALAD activity have been asses­ cytidine-5'-monophosphate to uridine sed by the measurement in blood and and cytidine liberating orthophosphate. urine of heme precursors and derivatives The enzyme is very sensitive to lead, and by clinical evaluation of the subject. being almost completely inhibited by a These parameters are themselves insen­ 10~6 M concentration (about 20 fig per sitive to lead toxicity, except for erythro­ dl). In lead-exposed subjects, having cyte protoporphyrin (FEP). Maxfield and blood lead concentrations between 44 Henry21 concluded, on the basis of exper­ and 109 fig per dl, the enzyme activity iments in which blood from non-exposed was markedly depressed. Further studies dogs was mixed with blood from dogs ex­ are required to determine the value of posed to lead, that the observed lowered this enzyme as an indicator of lead tox­ ALAD activity in exposed dogs was due icity. to an in vivo effect. ALAD activity
Load more

Recommended publications
  • Four Patients with Amanita Phalloides Poisoning CASE SERIE
    CASE SERIE 353 Four patients with Amanita Phalloides poisoning S. Vanooteghem1, J. Arts2, S. Decock2, P. Pieraerts3, W. Meersseman4, C. Verslype1, Ph. Van Hootegem2 (1) Department of hepatology, UZ Leuven ; (2) Department of gastroenterology, AZ St-Lucas, Brugge ; (3) General Practitioner, Zedelgem ; (4) Department of internal medicine, UZ Leuven. Abstract because they developed stage 2 hepatic encephalopathy. With maximal supportive therapy, all patients gradually Mushroom poisoning by Amanita phalloides is a rare but poten- improved from day 3 and recovered without the need for tially fatal disease. The initial symptoms of nausea, vomiting, ab- dominal pain and diarrhea, which are typical for the intoxication, liver transplantation. They were discharged from the can be interpreted as a common gastro-enteritis. The intoxication hospital between 6 to 10 days after admission. can progress to acute liver and renal failure and eventually death. Recognizing the clinical syndrome is extremely important. In this case report, 4 patients with amatoxin intoxication who showed the Discussion typical clinical syndrome are described. The current therapy of amatoxin intoxication is based on small case series, and no ran- Among mushroom intoxications, amatoxin intoxica- domised controlled trials are available. The therapy of amatoxin intoxication consists of supportive care and medical therapy with tion accounts for 90% of all fatalities. Amatoxin poison- silibinin and N-acetylcysteine. Patients who develop acute liver fail- ing is caused by mushroom species belonging to the gen- ure should be considered for liver transplantation. (Acta gastro- era Amanita, Galerina and Lepiota. Amanita phalloides, enterol. belg., 2014, 77, 353-356). commonly known as the “death cap”, causes the majority Key words : amanita phalloides, mushroom poisoning, acute liver of fatal cases.
    [Show full text]
  • Clinical Biochemistry of Hepatotoxicity
    linica f C l To o x l ic a o n r l o u g Singh, J Clinic Toxicol 2011, S:4 o y J Journal of Clinical Toxicology DOI: 10.4172/2161-0495.S4-001 ISSN: 2161-0495 ReviewResearch Article Article OpenOpen Access Access Clinical Biochemistry of Hepatotoxicity Anita Singh1, Tej K Bhat2 and Om P Sharma2* 1CSK Himachal Pradesh, Krishi Vishva Vidyalaya, Palampur (HP) 176 062, India 2Biochemistry Laboratory, Indian Veterinary Research Institute, Regional Station, Palampur (HP) 176 061, India Abstract Liver plays a central role in the metabolism and excretion of xenobiotics which makes it highly susceptible to their adverse and toxic effects. Liver injury caused by various toxic chemicals or their reactive metabolites [hepatotoxicants) is known as hepatotoxicity. The present review describes the biotransformation of hepatotoxicants and various models used to study hepatotoxicity. It provides an overview of pathological and biochemical mechanism involved during hepatotoxicity together with alteration of clinical biochemistry during liver injury. The review has been supported by a list of important hepatotoxicants as well as common hepatoprotective herbs. Keywords: Hepatotoxicity; Hepatotoxicant; In Vivo models; In Vitro production of bile thus leading to the body’s inability to flush out the models; Pathology; Alanine aminotransferase; Alkaline phosphatase; chemicals through waste. Smooth endoplasmic reticulum of the liver is Bilirubin; Hepatoprotective the principal ‘metabolic clearing house’ for both endogenous chemicals like cholesterol, steroid hormones, fatty acids and proteins, and Introduction exogenous substances like drugs and alcohol. The central role played by liver in the clearance and transformation of chemicals exposes it to Hepatotoxicity refers to liver dysfunction or liver damage that is toxic injury [4].
    [Show full text]
  • The Effect of Bacillus Larvicidal Toxins on Mammals
    The effect of Bacillus larvicidal toxins On mammals By Nadia Adam Mohammed Ahmed B.Sc. of Veterinary Sciences University of Bahr-Elgazal ٢٠٠٠ Thesis submitted for the partial fulfillment of the requirements For the degree of Master of Science (M.Sc.) in microbiology Supervisor Professor: Mohammed Sulieman El-sanosi Department of microbiology Faculty of Veterinary Medicine University of Khartoum ٢٠٠٦ May To My lovely parents, My husband (M/Elmurtada) and my children (Reem&Rwan) To My brothers and sisters, And To Those who suffer from malaria, I dedicate this work. Nadia I would like to express my sincere thanks to my supervisor Prof. Elsanosi for his valuable supervision and encouragement. I also like to extend my thanks to Prof.Ahamed.A.Gameel for his great help in histopathological investigation of this study. Thanks also extend to all staff and technicians of the Department of Microbiology for their valuable advices and assistance. Iam also greatfull to my colleague and all my friends Special thanks to my family for their patience and continuous encouragement during this work. Abstract Mosquito control is the key for hopeful and sustainable eradication of different socio-economic as well as fatal viral, bacterial and parasitological diseases in the tropical and subtropical countries. In addition the safety of any pesticide should be assured before application. In the present study the susceptibility of arabiensis mosquito larvae to the toxin of two endo-spores forming bacilli strain was examined. Both Bacilli spp B. ٪١٠٠ thuringiensis and B. sphaericus were found to be highly toxic and fatal with was found to be tolerant to the (٤_Instar) ٤_mortality rate.
    [Show full text]
  • Medications in Pregnant and Nursing Mothers
    Medications in Pregnant and Nursing Mothers NADINE M. GIRGIS, OD, FAAO ASSISTANT PROFESSOR YIN C. TEA, OD, FAAO CHIEF, PEDIATRICS AND BINOCULAR VISION ASSISTANT PROFESSOR Gestation age vs fetal age Gestation age-sperm penetrates the egg and zygote is formed Zygote (fertilized egg) travels from fallopian tube to uterus During this time, egg divides into cells - called a morula Continued dividing and morula - called a blastocyst - embeds in the uterus anywhere from 6-12 days after conception This begins the embryonic stage and fetal age begins Fetal development-1st trimester Gestation age week 3-fetal age week 1: a lot of basic growth Brain, spinal cord, heart, GI tract begin development 1st trimester Gestation age-week 4 and 5: embryo ¼ inch long Arm and leg buds, ears, eyes forming Placenta forming and producing hormones Heart is beating at a steady rhythm Movement of rudimentary blood through blood vessels 1st trimester Gestation age week 6: embryo is ½ in length Lungs, jaw, nose, plate formation, hands and feet Hand and feet buds have webbed structures Brain forming into complex parts 1st trimester Gestation age week 7: weighs less than an aspirin All essential organs have begun to form Hair, nail follicles, eyelids and tongue starting to form Trunk begins to straighten out 1st trimester Gestation age week 8: 1 in long, size of a bean All parts of adult are now present in the embryo Bones beginning to form Muscles begin to contract Facial features, including eyelids more developed Gestation age weeks 9-13: 3 in and weighs
    [Show full text]
  • Research Article Presentations Related to Acute
    Hindawi Emergency Medicine International Volume 2019, Article ID 3130843, 7 pages https://doi.org/10.1155/2019/3130843 Research Article Presentations Related to Acute Paracetamol Intoxication in an Urban Emergency Department in Switzerland Natalia Piotrowska,1 Jolanta Klukowska-Ro¨tzler ,1 Beat Lehmann ,1 Gert Krummrey,1 Manuel Haschke,2,3 Aristomenis K. Exadaktylos,1 and Evangelia Liakoni 2,3 1Department of Emergency Medicine, Inselspital, University Hospital Bern, University of Bern, Bern, Switzerland 2Clinical Pharmacology and Toxicology, Department of General Internal Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland 3Institute of Pharmacology, University of Bern, Bern, Switzerland Correspondence should be addressed to Evangelia Liakoni; [email protected] Received 25 March 2019; Accepted 22 November 2019; Published 6 December 2019 Academic Editor: $eodore J. Gaeta Copyright © 2019 Natalia Piotrowska et al. $is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim. To investigate the characteristics of Emergency Department (ED) presentations due to acute paracetamol intoxication. Methods. Retrospective observational study of patients presenting to the ED of Bern University Hospital between May 1, 2012, and October 31, 2018, due to a paracetamol overdose (defined as intake of >4 g/24 h). Cases were identified using the full-text search of the electronic patient database and were grouped into intentional (suicidal/parasuicidal) and unintentional in- toxications (e.g., patient unaware of maximal daily dose). Results. During the study period, 181 cases were included and 143 (79%) of those were intentional.
    [Show full text]
  • Ethanol and Tobacco Abuse in Pregnancy: Anaesthetic Considerations
    REVIEW ARTICLE Ethanol and tobacco abuse in pregnancy: Anaesthetic considerations K M Kuczkowski M.D, Assistant Clinical Professor of Anesthesiology and Reproductive Medicine, Co-Director of Obstetric Anesthesia, Departments of Anesthesiology and Reproductive Medicine, University of California, San Diego , USA Introduction The illicit drug abuse in pregnancy has received significant attention over the past two decades.1 However, far too little attention has been given to the consequences of the use of social drugs such as ethanol and tobacco, which are by far the most commonly abused substances during pregnancy. While the deleterious effects of cocaine or amphetamines on the mother and the fetus are more pronounced and easier to detect, the addiction to ethanol and tobacco is usually subtle and more difficult to diagnose.1, 2-4 As a result recreational use of alcohol and tobacco may continue undetected in pregnancy, significantly effecting pregnancy outcome and obstetric and anaesthetic management of these patients. This article reviews the consequences of ethanol and tobacco use in pregnancy and offers recommendation for anaesthetic management of these potentially complicated pregnancies. General considerations rette smoking.2, 17 The American College of Obstetricians and Substance abuse is defined as “self-administration of various drugs Gynaecologists (ACOG) has made multiple recommendations regard- that deviates from medically or socially accepted use, which if pro- ing management of patients with drug abuse during pregnancy. longed can lead to the development of physical and psychological Women who acknowledge use of illicit substance during pregnancy dependence”.5 This chemical dependency is characterized by peri- should be counseled and offered necessary treatment.
    [Show full text]
  • The Nervous System – Target Organ Into the Twenty-First Century
    The Nervous System – Target Organ into the Twenty-First Century R. Douglas Hamm MD, CCFP, FRCPC (Occ Med), FCBOM President, Canadian Board of Occupational Medicine CONTENTS 1. WHY NEURONS MAKE GOOD TARGETS FOR OCCUPATIONAL TOXICANTS 2. FROM CLASSICAL PLUMBISM TO BEHAVIORAL TOXICOLOGY 3. TOXICOKINETICS, COMPARTMENTS, AND PBPK MODELS 4. THE DIVERSE TOXICODYNAMICS OF THE NERVOUS SYSTEM 1. Peripheral Neurons (neuronopathy, axonopathy, myelinopathy) 2. Synaptic Neurotransmission (cholinergic pathways) 3. Special Senses (visual, auditory, olfactory) 4. Movement Disorders (parkinsonism, ataxia, tremor) 5. Neuroaffective and Neurocognitive Effects 5. NOTEWORTHY OCCUPATIONAL NEUROTOXICANTS 1. “Heavy metals” (Pb, Hg, Tl) and other elements (Mn, As, Al, Sb, Te) 2. Organic Solvents (toluene, xylene, styrene, C2HCl3, C2Cl4, CH3CCl3, CS2) 3. Gases (HCN, CO, H2S, ethylene oxide) 4. Pesticides (organophosphates, carbamates, organochlorines, pyrethroids, neonicotinoids) 6. CLINICAL NEUROTOXICOLOGY 1. Identification of Occupational Neurotoxic Disorders 2. Biomarkers of Exposure and Effect 3. Clinical Investigations of Neurotoxicity 1. WHY NEURONS MAKE GOOD 2. FROM CLASSICAL PLUMBISM TO TARGETS FOR OCCUPATIONAL BEHAVIORAL TOXICOLOGY TOXICANTS Hippocrates (c. 460-370 BC) has been cited as Neuroanatomical structures have large surface the first ancient author to describe a case of areas and receptor populations, e.g., the occupational neurotoxicity but this has been surface area of the brain’s 100 billion neurons shown to be erroneous (Osler, 1907; Waldron, totals hundreds of square metres. 1973, 1978; Skrabanek, 1986; Vance, 2007). The earliest report appears to be that of Neurons have high rates of metabolism, e.g., Nicander of Colophon (2nd cent. BC) who the brain at 2% body mass consumes 20% of observed that in “psimuthion” i.e.
    [Show full text]
  • Results of Liver Transplantation in Patients with Acute Liver Failure Due to Amanita Phalloides and Paracetamol (Acetaminophen) Intoxication
    Original paper Results of liver transplantation in patients with acute liver failure due to Amanita phalloides and paracetamol (acetaminophen) intoxication Maciej Krasnodębski, Michał Grąt, Wacław Hołówko, Łukasz Masior, Karolina M. Wronka, Karolina Grąt, Jan Stypułkowski, Waldemar Patkowski, Marek Krawczyk Department of General, Transplant, and Liver Surgery, Medical University of Warsaw, Warsaw, Poland Gastroenterology Rev 2016; 11 (2): 90–95 DOI: 10.5114/pg.2015.52031 Key words: acute liver failure, Amanita phalloides poisoning, paracetamol poisoning, liver transplantation. Address for correspondence: Maciej Krasnodębski MD, Department of General, Transplant, and Liver Surgery, Medical University of Warsaw, 1 A Banacha St, 02-097 Warsaw, Poland, phone: +48 22 599 25 45, fax: +48 22 599 15 45, e-mail: [email protected] Abstract Introduction: Amanita phalloides and paracetamol intoxications are responsible for the majority of acute liver failures. Aim: To assess survival outcomes and to analyse risk factors affecting survival in the studied group. Material and methods: Of 1369 liver transplantations performed in the Department of General, Transplant, and Liver Sur- gery, Medical University of Warsaw before December 2013, 20 (1.46%) patients with Amanita phalloides (n = 13, 0.95%) and paracetamol (n = 7, 0.51%) intoxication were selected for this retrospective study. Overall and graft survival at 5 years were set as primary outcome measures. Results: Five-year overall survival after liver transplantation in the studied group was 53.57% and 53.85% in patients with paracetamol and Amanita phalloides poisoning, respectively (p = 0.816). Five-year graft survival was 26.79% for patients with paracetamol and 38.46% with Amanita phalloides intoxication (p = 0.737).
    [Show full text]
  • Preferred Drug List
    October 2021 Preferred Drug List The Preferred Drug List, administered by CVS Caremark® on behalf of Siemens, is a guide within select therapeutic categories for clients, plan members and health care providers. Generics should be considered the first line of prescribing. If there is no generic available, there may be more than one brand-name medicine to treat a condition. These preferred brand-name medicines are listed to help identify products that are clinically appropriate and cost-effective. Generics listed in therapeutic categories are for representational purposes only. This is not an all-inclusive list. This list represents brand products in CAPS, branded generics in upper- and lowercase Italics, and generic products in lowercase italics. PLAN MEMBER HEALTH CARE PROVIDER Your benefit plan provides you with a prescription benefit program Your patient is covered under a prescription benefit plan administered administered by CVS Caremark. Ask your doctor to consider by CVS Caremark. As a way to help manage health care costs, prescribing, when medically appropriate, a preferred medicine from authorize generic substitution whenever possible. If you believe a this list. Take this list along when you or a covered family member brand-name product is necessary, consider prescribing a brand name sees a doctor. on this list. Please note: Please note: • Your specific prescription benefit plan design may not cover • Generics should be considered the first line of prescribing. certain products or categories, regardless of their appearance in • This drug list represents a summary of prescription coverage. It is this document. Products recently approved by the U.S. Food and not all-inclusive and does not guarantee coverage.
    [Show full text]
  • Transdermal Methyl Alcohol Intoxication: a Case Report
    Acta Derm Venereol 2015; 95: 740–741 SHORT COMMUNICATION Transdermal Methyl Alcohol Intoxication: A Case Report Burcu Hizarci, Cem Erdoğan, Pelin Karaaslan, Aytekin Unlukaplan and Huseyin Oz Department of Anesthesiology and Reanimation, Medipol University Medical Faculty, Istanbul, Turkey. E-mail: [email protected] Accepted Jan 8, 2015; Epub ahead of print Jan 9, 2015 Methyl alcohol (methanol) is a colourless, odourless visual disorder gradually improved during the period and bitter substance found in solvents, paint removers, he was observed in the intensive care unit. His cranial varnish es, antifreezes, cologne and grain alcohol (1). imagings revealed no abnormality. Bicarbonate infu- Methanol is a central nervous system depressant that is sion was discontinued after 24 h as metabolic acidosis potentially toxic after its ingestion, inhalation or transder- had normalised. After 72 h of monitoring, the patient mal exposure (1–4). Most of the patients have headache, was discharged after stabilisation. nausea, vomiting, weakness and vision loss during this period. As a result of high intake, the patient presents DISCUSSION with stupor, coma and even death. Although methanol in- toxication is most frequently reported due to oral intake, After oral intake methanol is converted to formalde- cases of inhalation and transdermal methanol intoxication hyde in the liver and oxidised to formic acid. Formic are reported as well (5). In this paper we report a rare acid is toxic for central nervous system and as a result, case of transdermal methanol intoxication. We suggest histological hypoxia, which is caused by axonal cell that transdermal toxication should be considered and death occurs (6). Percutaneous exposure of methanol questioned whilst taking the medical history of a patient.
    [Show full text]
  • Specific Pattern of Gene Expression During Induction of Mouse Erythroleukemia Cells
    Downloaded from genesdev.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Specific pattern of gene expression during induction of mouse erythroleukemia cells Peter J. Fraser and Peter J. Curtis The Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104 USA We have studied the expression of several characterized genes during induction of mouse erythroleukemia (MEL) cells with dimethyl sulfoxide (DMSO) and have observed a specific pattern of changes in transcriptional activity and steady-state RNA levels associated with erythroid differentiation. During induction there is a gradual, steady decrease in total transcriptional activity and RNA content per cell, which by day 3 of DMSO treatment amounts to less than 50% of the level in the uninduced cell. During this time we observe increases in transcriptional activity for 5-aminolevulinic acid synthase, carbonic anhydrase form II, and band 3 coordinate with the large increase in [3-globin gene transcription. The results also demonstrate an early decrease in transcription for carbonic anhydrase form I, which precedes decreases in transcription for glyceraldehyde phosphate dehydrogenase and rRNA genes. Changes in steady-state RNA levels reflected changes in transcriptional activity during induction except for carbonic anhydrase II mRNA. These results represent the first report characterizing the regulated expression at transcriptional and posttranscriptional levels of several known genes that are characteristically expressed in the erythrocyte. The results demonstrate that coordinate gene expression in erythroid differentiation occurs primarily at the level of transcription. [Key Words: Coordinated gene regulation; transcriptional activity; erythroid differentiation] Received June 25, 1987; revised version accepted August 14, 1987. Adult erythroid differentiation requires activation and/ dinately such that they may assemble to form the char- or modulation of many genes whose expression is regu- acteristic erythrocyte cytoskeleton.
    [Show full text]
  • Table S1. the Bacterial and Fungal Isolates Used for the in Vitro Activity Testing
    Table S1. The bacterial and fungal isolates used for the in vitro activity testing. KTU-286 Microorganism Strain No Feature MIC (µg/mL) Acinetobacter baummanii ATCC 17978 Reference strain 128 < Aspergillus flavus 12B Clinical isolate 128 < Aspergillus fumigatus 14 Clinical isolate 128 < Candida albicans ATCC 10231 Type strain 128 < Candida auris CAU-1 Clinical isolate 128 < Cuninghamella corymbifera CC1 Clinical isolate 128 < Escherichia coli 10025 Mcr-1 128 Escherichia coli DH5a Pan-S 128 Klebsiella pneumoniae 3122 blaKPC 128 < Klebsiella pneumoniae 4141 blaNDM-1 128 < Mycobacterium abscesus IP-K01 Clinical isolate 64 Mycobacterium bovis BCG Type strain 128 < Mycobacterium smegmatis mc2155 Type strain 128 < Pseudomonas aeruginosa 3691 AmpC 128 < Pseudomonas aeruginosa 3656 Pan-S 128 < Pseudomonas aeruginosa 3647 Efflux pump overexpression 128 < Pseudomonas aeruginosa 3619 OPRD 128 < Staphylococcus aureus 875 MRSA 1 Table S2. The In silico predictions of human proteins interacting with KTU-286. The in silico predictions were computed using SwissTargetPrediction tool. Common Uniprot ChEMBL Probab Identified target Target Class name ID ID ility CHEMBL2 0.10057 Arachidonate 5-lipoxygenase ALOX5 P09917 Oxidoreductase 15 8902 CHEMBL5 0.10057 Prostaglandin E synthase PTGES O14684 Enzyme 658 8902 CHEMBL2 Family A G protein- 0.10057 Interleukin-8 receptor B CXCR2 P25025 434 coupled receptor 8902 CHEMBL2 0.10057 Cyclooxygenase-2 PTGS2 P35354 Oxidoreductase 30 8902 CHEMBL3 0.10057 Carboxylesterase 2 CES2 O00748 Enzyme 180 8902 CHEMBL5 0.10057 Poly
    [Show full text]