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Statements

Subject Item
n2:RIV%2F00216208%3A11140%2F13%3A10139295%21RIV14-MSM-11140___
rdf:type
n8:Vysledek skos:Concept
dcterms:description
Background. Thioacetamide (TAA), a well known inducer of hepatic fibrosis, has been often used in experimental acute and chronic hepatotoxicity models. Reactive oxygen species play an important role in TAA-induced liver damage. Aims. To study the time course of activities of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of rats after chronic TAA administration. Methods. Female Wistar rats were treated with TAA (intraperitoneally, 200 mg/kg body weight) for 12 weeks, the controls received saline. Animals were sacrificed 4, 12 or 16 weeks after the treatment discontinuation. Lipid peroxidation (LP), reduced glutathione (GSH) and activities of glutathione peroxidase (GPx), glutathione reductase (GR) and katalase (CAT) were estimated in the liver and kidneys. ALT, AST and GLDH were measured in serum. Results. Significant increases in serum ALT and GLDH persisted for 16 weeks ater the treatment, while serum AST was increased only in animals sacrificed 4 weeks after the treatment cessation. No increase in LP or decrease in GSH was observed in the liver. Furthermore, a decrease in LP and an increase in GR activity appeared in the 16th week. Significant decreases in the activities of catalase and GPx (which persisted in animals sacrificed 12 and 16 weeks after the treatment, respectively) were the only markers of hepatic oxidative damage. In kidneys, LP was significantly increased 4 and 12 weeks after the TAA treatment which implies the importance of oxidative stress in the renal damage that develops as a consequence of liver cirrhosis. Background. Thioacetamide (TAA), a well known inducer of hepatic fibrosis, has been often used in experimental acute and chronic hepatotoxicity models. Reactive oxygen species play an important role in TAA-induced liver damage. Aims. To study the time course of activities of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of rats after chronic TAA administration. Methods. Female Wistar rats were treated with TAA (intraperitoneally, 200 mg/kg body weight) for 12 weeks, the controls received saline. Animals were sacrificed 4, 12 or 16 weeks after the treatment discontinuation. Lipid peroxidation (LP), reduced glutathione (GSH) and activities of glutathione peroxidase (GPx), glutathione reductase (GR) and katalase (CAT) were estimated in the liver and kidneys. ALT, AST and GLDH were measured in serum. Results. Significant increases in serum ALT and GLDH persisted for 16 weeks ater the treatment, while serum AST was increased only in animals sacrificed 4 weeks after the treatment cessation. No increase in LP or decrease in GSH was observed in the liver. Furthermore, a decrease in LP and an increase in GR activity appeared in the 16th week. Significant decreases in the activities of catalase and GPx (which persisted in animals sacrificed 12 and 16 weeks after the treatment, respectively) were the only markers of hepatic oxidative damage. In kidneys, LP was significantly increased 4 and 12 weeks after the TAA treatment which implies the importance of oxidative stress in the renal damage that develops as a consequence of liver cirrhosis.
dcterms:title
The influence of chronic administration of thioacetamide on levels of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of female Wistar rats The influence of chronic administration of thioacetamide on levels of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of female Wistar rats
skos:prefLabel
The influence of chronic administration of thioacetamide on levels of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of female Wistar rats The influence of chronic administration of thioacetamide on levels of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of female Wistar rats
skos:notation
RIV/00216208:11140/13:10139295!RIV14-MSM-11140___
n8:predkladatel
n19:orjk%3A11140
n4:aktivita
n13:S n13:P n13:I
n4:aktivity
I, P(ED2.1.00/03.0076), S
n4:cisloPeriodika
Supplement 1
n4:dodaniDat
n16:2014
n4:domaciTvurceVysledku
n10:1385356 n10:6980902 n10:8535035 n10:6361846
n4:druhVysledku
n12:J
n4:duvernostUdaju
n18:S
n4:entitaPredkladatele
n15:predkladatel
n4:idSjednocenehoVysledku
79698
n4:idVysledku
RIV/00216208:11140/13:10139295
n4:jazykVysledku
n9:eng
n4:klicovaSlova
rat; aminotrasferases; oxidative stress; kidney; liver; thioacetamide
n4:klicoveSlovo
n7:kidney n7:liver n7:rat n7:aminotrasferases n7:thioacetamide n7:oxidative%20stress
n4:kodStatuVydavatele
CZ - Česká republika
n4:kontrolniKodProRIV
[1CDDF9AF074C]
n4:nazevZdroje
Biomedical Papers
n4:obor
n6:FR
n4:pocetDomacichTvurcuVysledku
4
n4:pocetTvurcuVysledku
4
n4:projekt
n11:ED2.1.00%2F03.0076
n4:rokUplatneniVysledku
n16:2013
n4:svazekPeriodika
157
n4:tvurceVysledku
Mistrová, Eliška Bludovská, Monika Kotyzová, Dana Chottová-Dvořáková, Magdaléna
n4:wos
000324728600005
s:issn
1213-8118
s:numberOfPages
5
n17:organizacniJednotka
11140