Changes in glucose-6-phosphate dehydrogenase and malic enzyme gene expression in acute hepatic injury induced by thioacetamide

NADPH-generating enzymes, glucose-6-phosphate dehydrogenase (G6PDH), and malic enzyme (ME) were studied in rat liver when necrosis and regeneration were induced by a single sublethal dose of thioacetamide (6.6 mmol/kg). Both enzyme activities decreased sharply at 12–24 hr of treatment and increased...

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Published inBiochemical pharmacology Vol. 51; no. 9; pp. 1159 - 1163
Main Authors Díez-Fernández, Carmen, Sanz, Nuria, Cascales, María
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 03.05.1996
Elsevier Science
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Abstract NADPH-generating enzymes, glucose-6-phosphate dehydrogenase (G6PDH), and malic enzyme (ME) were studied in rat liver when necrosis and regeneration were induced by a single sublethal dose of thioacetamide (6.6 mmol/kg). Both enzyme activities decreased sharply at 12–24 hr of treatment and increased thereafter. These biphasic changes are related to the sequential processes of liver injury and hepatocellular regeneration. Expression of mRNA for G6PDH decreased at 12 hr following thioacetamide injection and increased during liver regeneration, reaching its highest levels of expression at 48 hr (247% of the control), parallel to the peak of DNA synthesis. Expression of ME decreased at 12–24 hr and increased during the postnecrotic regenerating process, reaching only half of the control value at 96 hr. A relationship between mRNA G6PDH gene expression, oxidative stress (detected by the GSH/GSSG ratio and malondialdehyde (MDA) concentration), and DNA synthesis is proposed.
AbstractList NADPH-generating enzymes, glucose-6-phosphate dehydrogenase (G6PDH), and malic enzyme (ME) were studied in rat liver when necrosis and regeneration were induced by a single sublethal dose of thioacetamide (6.6 mmol/kg). Both enzyme activities decreased sharply at 12-24 hr of treatment and increased thereafter. These biphasic changes are related to the sequential processes of liver injury and hepatocellular regeneration. Expression of mRNA for G6PDH decreased at 12 hr following thioacetamide injection and increased during liver regeneration, reaching its highest levels of expression at 48 hr (247% of the control), parallel to the peak of DNA synthesis. Expression of ME decreased at 12-24 hr and increased during the postnecrotic regenerating process, reaching only half of the control value at 96 hr. A relationship between mRNA G6PDH gene expression, oxidative stress (detected by the GSH/GSSG ratio and malondialdehyde (MDA) concentration), and DNA synthesis is proposed.
Author Cascales, María
Díez-Fernández, Carmen
Sanz, Nuria
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Issue 9
Keywords NADPH-generating enzymes
necrosis
regeneration
G6PDH
ME
MDA
gene expression
oxidative stress
Oxidative stress
Glucose-6-phosphate 1-dehydrogenase
Rat
Enzyme
Liver
Rodentia
Hepatic disease
)
Gene expression
Mechanism
Malate dehydrogenase (oxaloacetate-decarboxylating) (NADP
Necrosis
Regeneration
Vertebrata
Experimental disease
Mammalia
Digestive diseases
Oxidoreductases
Language English
License CC BY 4.0
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PublicationTitle Biochemical pharmacology
PublicationTitleAlternate Biochem Pharmacol
PublicationYear 1996
Publisher Elsevier Inc
Elsevier Science
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Snippet NADPH-generating enzymes, glucose-6-phosphate dehydrogenase (G6PDH), and malic enzyme (ME) were studied in rat liver when necrosis and regeneration were...
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SubjectTerms Animals
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
gene expression
Gene Expression Regulation, Enzymologic - drug effects
Glucosephosphate Dehydrogenase - genetics
Liver - drug effects
Liver - injuries
Liver. Bile. Biliary tracts
Malate Dehydrogenase - genetics
Male
NADPH-generating enzymes
necrosis
Oxidative Stress
Rats
Rats, Wistar
regeneration
RNA, Messenger - genetics
RNA, Messenger - metabolism
Thioacetamide - toxicity
Vertebrates: digestive system
Title Changes in glucose-6-phosphate dehydrogenase and malic enzyme gene expression in acute hepatic injury induced by thioacetamide
URI https://dx.doi.org/10.1016/0006-2952(96)00030-5
https://www.ncbi.nlm.nih.gov/pubmed/8645338
Volume 51
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