• MeSH
• azathioprin škodlivé účinky   MeSH
• cyklofosfamid škodlivé účinky   MeSH
• lékové postižení jater * MeSH
• lidé MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• azathioprin MeSH
• cyklofosfamid MeSH

From the accessible material an attempt was made to estimate the frequency of acute toxic disturbances of liver and its relation to all intoxications together with special regard to the composition of noxious substances on the conditions of this country. From 3700 cases of all acute intoxications or serious attempts of intoxication 54 cases were discovered to have marked hepatic disturbance (about 1.5%). The noxious substance causing hepatic disturbance in the overwhelming majority of cases was tetrachlormethan (and chemically related substances) or new herbicide drugs of the dipyridine compounds. The last mentioned group is highly lethal and the more important as it is a relatively new substance to which health control and practice is less accustomed as to a potential hepatotoxic drug than to tetrachlormethan. It is pointed further to a less frequent potential intoxication by phenylbutazone and its derivatives especially in children and to the acute intoxication by INH when high single doses of this drug are used.

• MeSH
• akutní nemoc MeSH
• fenoly otrava   MeSH
• fenylbutazon otrava   MeSH
• isoniazid otrava   MeSH
• kojenec MeSH
• lékové postižení jater * MeSH
• lidé MeSH
• nemoci z povolání epidemiologie   MeSH
• otrava epidemiologie   MeSH
• paraquat otrava   MeSH
• předškolní dítě MeSH
• registrace MeSH
• Check Tag
• kojenec MeSH
• lidé MeSH
• předškolní dítě MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Československo MeSH
• Názvy látek
• fenoly MeSH
• fenylbutazon MeSH
• isoniazid MeSH
• paraquat MeSH

• MeSH
• antihypertenziva škodlivé účinky   terapeutické užití   MeSH
• benzopyrany terapeutické užití   MeSH
• chromany (dihydrobenzopyrany) škodlivé účinky   terapeutické užití   MeSH
• guanidiny škodlivé účinky   terapeutické užití   MeSH
• hodnocení léčiv MeSH
• hypertenze farmakoterapie   MeSH
• klinické zkoušky jako téma MeSH
• lékové postižení jater MeSH
• lidé MeSH
• nemoci kostní dřeně chemicky indukované   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• klinické zkoušky MeSH
• Názvy látek
• antihypertenziva MeSH
• benzopyrany MeSH
• chromany (dihydrobenzopyrany) MeSH
• guanidiny MeSH

• Klíčová slova
• ADOLESCENCE *, CHOLINESTERASE INHIBITORS *, HEPATITIS, TOXIC *, PSYCHOSES, TOXIC *, PYROPHOSPHATES *, TOXICOLOGIC REPORT *,
• MeSH
• cholinesterasové inhibitory * MeSH
• difosfáty * MeSH
• hepatitida A * MeSH
• hepatitida * MeSH
• lékové postižení jater * MeSH
• mladiství MeSH
• psychotické poruchy * MeSH
• toxické psychózy * MeSH
• toxikologie * MeSH
• Check Tag
• mladiství MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• cholinesterasové inhibitory * MeSH
• difosfáty * MeSH

• Klíčová slova
• BLOOD CELLS *, DERMATITIS MEDICAMENTOSA *, DRUG HYPERSENSITIVITY *, HEPATITIS, TOXIC *, MYOCARDITIS *, PSYCHOSES, TOXIC *, REVIEW *, STEVENS-JOHNSON SYNDROME *, SULFAMETHOXYPYRIDAZINE *, TOXICOLOGIC REPORT *,
• MeSH
• hepatitida A * MeSH
• hepatitida * MeSH
• krevní buňky * MeSH
• léková alergie * MeSH
• léková dermatitida * MeSH
• lékové postižení jater * MeSH
• myokarditida * MeSH
• psychotické poruchy * MeSH
• Stevensův-Johnsonův syndrom * MeSH
• sulfamethoxypyridazin * MeSH
• toxické psychózy * MeSH
• toxikologie * MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• sulfamethoxypyridazin * MeSH

OBJECTIVES: Previous studies using oral administration of environmentally relevant doses of cyanobacterial biomass containing microcystins (MCs) induced only sub-lethal effects in experimental birds. Therefore, the objective of this study was to obtain data on avian high-dose toxicity of MCs and compute LD50, if possible, following the natural oral route of administration. DESIGN: Responses of birds to single high-dose exposure to MCs were evaluated in fourteen-day old Japanese quail males (Coturnix coturnix japonica) with average body weight of 50 g which were randomly divided into five groups. Birds from four experimental groups were administered 7.5 ml of cyanobacterial biomass suspension containing increasing MCs quantities of 2500, 5000, 10000, and 20000 µg/kg using oral gavage. Controls received an equal dose of drinking water instead of the test substance. Birds were observed for clinical signs of acute toxicity. Survivors were killed on day 5 to obtain body and liver weights. A five-grade semi-quantitative system for histopathological liver damage scoring was used to compare cyanobacterial-biomass-exposed birds against controls. RESULTS: No mortality occurred during the period of five days post exposure in both control and MCs-exposed groups and this high-dose experiment failed to provide data to compute the LD50. Nevertheless, marked sub-lethal effects were recognised in the damage of liver that included dose-dependent changes in the body/liver ratios and morphological changes ranging from mild vacuolar dystrophy to focal liver necroses in the highest exposure group. Hepatic lesions were mainly observed in the pericentral area of the liver. CONCLUSIONS: Though maximum cyanobacterial biomass dose rates that could be administered to birds of the size were used in the present experiment and more pronounced hepatic lesions than after exposure to environmentally relevant doses were observed, birds would probably have survived unless killed for histopathology on day 5 of exposure. These results provide support to previously reported data on sub-lethal effects following exposure to cyanobacterial biomass containing MCs in birds and mortality occurring only in birds under combined action with other stressors.

• MeSH
• bakteriální toxiny toxicita   MeSH
• biomasa MeSH
• Coturnix * MeSH
• hepatocyty účinky léků   patologie   MeSH
• karcinogeny toxicita   MeSH
• LD50 MeSH
• lékové postižení jater epidemiologie   patologie   MeSH
• mikrocystiny toxicita   MeSH
• mořské toxiny toxicita   MeSH
• náhodné rozdělení MeSH
• rizikové faktory MeSH
• sinice chemie   MeSH
• tělesná hmotnost MeSH
• toxiny kmene Cyanobacteria MeSH
• velikost orgánu MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• bakteriální toxiny MeSH
• karcinogeny MeSH
• mikrocystiny MeSH
• mořské toxiny MeSH
• toxiny kmene Cyanobacteria MeSH

Thioacetamide (TAA) is a hepatotoxin frequently used for experimental purposes which produces centrilobular necrosis after a single dose administration. In spite of the fact that oxidative stress seems to play a very important role in the mechanism of TAA-induced injury, the effect of TAA on hepatocytes in primary culture with respect to the influence on mitochondria has yet to be verified. Hepatocytes were incubated for 24h in a medium containing TAA (0-70 mmol/l). Glutathione content (GSH/GSSG), reactive oxygen species and malondialdehyde formation were assessed as markers of cell redox state. Toxicity was determined by lactate dehydrogenase leakage and WST-1 assay. The functional capacity of hepatocytes was evaluated from albumin and urea production. Mitochondrial metabolism was assessed by measuring mitochondrial membrane potential and oxygen consumption. Our results show that a profound decrease in the GSH level in hepatocytes precedes a sharp rise in endogenous ROS production. ROS production correlates with an increase in lipoperoxidation. Mitochondria are affected by TAA secondarily as a consequence of oxidative stress. Oxidation of the NADH-dependent substrates of respiratory Complex I is significantly more sensitive to the toxic action of TAA than oxidation of the flavoprotein-dependent substrate of Complex II. Mitochondria can also maintain their membrane potential better when they utilize succinate as a respiratory substrate. It appears that GSH should be depleted below a certain critical level in order to cause a marked increase in lipid peroxidation. Mitochondrial injury can then occur and cell death develops.

• MeSH
• hepatocyty účinky léků   metabolismus   MeSH
• játra účinky léků   metabolismus   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• L-laktátdehydrogenasa metabolismus   MeSH
• lékové postižení jater metabolismus   MeSH
• malondialdehyd metabolismus   MeSH
• membránový potenciál mitochondrií účinky léků   MeSH
• nebezpečné látky toxicita   MeSH
• oxidační stres MeSH
• potkani Wistar MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• thioacetamid toxicita   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• L-laktátdehydrogenasa MeSH
• malondialdehyd MeSH
• nebezpečné látky MeSH
• reaktivní formy kyslíku MeSH
• thioacetamid MeSH