MMSL, 2011 (vol. 80), issue 3

ACUTE TOXICITY OF SODIUM SELENITE IN RODENTS: PATHOMORPHOLOGICAL STUDYOriginal article

Vesna Jacevic, Goran Jokic, Viktorija Dragojevic-Simic, Dubravko Bokonjic, Slavica Vucinic, Marina Vuksa

MMSL 2011, 80(3):90-96 | DOI: 10.31482/mmsl.2011.015  

The purpose of this study was to investigate the acute toxicity of sodium selenite in mice and rats after per os application to establish the relationship between a high toxic dose of sodium selenite and tissue alterations in rats. Increasing doses of sodium selenite (4, 10, 14 and 18 mg/kg) were administered in separate groups of mice and rats. Obtained LD₅₀ values of sodium selenite in mice and rats were in the range of 8.08 to 12.11 mg/kg po. In separate groups of rats of both genders, sodium selenite in a dose of 10 mg/kg po was applied. Survived animals were sacrificed after the end of day 7 and an increase of fluids...

HUMAN SERUM BUTYRYLCHOLINESTERASE AS A PROPHYLAXIS AGAINST RUSSIAN VXOriginal article

Jana Žďárová Karasová, Kamil Kuča, Daniel Jun, Jiří Bajgar

MMSL 2011, 80(3):97-102 | DOI: 10.31482/mmsl.2011.016  

Human serum butyrylcholinesterase (BChE, EC 3.1.1.8) is currently under advanced development as a pretreatment for organophosphorus (OP) poisoning in human. It was shown to protect mice, rats, guinea pigs, and monkeys against multiple LD₅₀ challenges of OPs nerve agents intoxications. The aim of this study was to verify the efficacy of the pretreatment by the human BChE in blood and brain after intramuscular intoxication by Russian VX agent (RVX). Purified human BChE was administered intraperitoneally (500 U/kg) 30 minutes before a single dose of RVX corresponding to 1 LD₅₀ (15 μg/kg). Changes in cholinesterases activities...

BIOMARKERS OF CARDIAC INJURY IN DETECTION OF CARDIOTOXICITY INDUCED BY CHEMOTHERAPEUTIC AGENTSReview article

Jan M. Horáček

MMSL 2011, 80(3):103-117 | DOI: 10.31482/mmsl.2011.017  

Cardiotoxicity is a well-known and potentially serious complication of oncology treatment. Anthracyclines and high-dose chemotherapy especially regimens containing high-dose Cyclophosphamide represent the greatest risk. Early detection of cardiotoxicity is crucial for applying preventive and supportive therapeutic strategies. Various methods have been recommended for monitoring of cardiotoxicity. In our conditions, echocardiography and electrocardiography are routinely used. However, this approach shows low sensitivity for the early prediction of cardiomyopathy when the possibilities of appropriate management could still improve the patient's outcome.Recently,...

THE DISULFIDE BOND FORMATION AND ITS RELATIONSHIP TO BACTERIAL PATHOGENICITY OF THREE IMPORTANT GRAM-NEGATIVE BACTERIAReview article

Iva Šenitková, Petra Špidlová, Lenka Hernychová, Jiří Stulík

MMSL 2011, 80(3):118-128 | DOI: 10.31482/mmsl.2011.018  

Disulfide bond formation is necessary for a correct folding and a proper function of many secreted proteins. We know that many of these proteins are involved in bacterial virulence and pathogenesis. The best known pathways of disulfide bond formation and isomerization belong to Escherichia coli (E. coli). This Gram-negative bacterium is usually used as a model organism. This review is aimed initially at introduction to E. coli oxido-reductase enzymatic system. The next part is interested in proteins resembling these from E. coli and their relation to virulence and pathogenesis. We have choosen three important Gram-negative...

ANATOXIN-A(S): NATURAL ORGANOPHOSPHORUS ANTICHOLINESTERASE AGENTReview article

Jiří Patočka, Ramesh C. Gupta, Kamil Kuča

MMSL 2011, 80(3):129-139 | DOI: 10.31482/mmsl.2011.019  

Anatoxin-a(s) is a guanidinemethyl phosphate ester isolated from the freshwater cyanobacterium (blue-green algae) Anabaena flos-aquae strain NRC 525-17. Previous work has shown anatoxin-a(s) to be a potent irreversible inhibitor of electric eel acetylcholinesterase (AChE, EC 3.1.1.7). Anatoxin-a(s) has been shown to be an active site-directed inhibitor of AChE, which is resistant to reactivation by oximes because of the enzyme-oxime adduct formation. In vivo pretreatment with physostigmine and high concentrations of pyridine 2-aldoxime methochloride (2-PAM) were the only effective antagonists against a lethal dose of anatoxin-a(s). Anatoxin-a(s)...