ArticleMolecular and cellular biochemistry2002
The expression of gamma-glutamyltransferase in rat colon carcinoma cells is distinctly regulated during differentiation and oxidative stress.
Article in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 16 citations in OpenAlex.
- A de novo strategy to develop NIR precipitating fluorochrome for long-term in situ cell membrane bioimaging.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Gamma-glutamyl transpeptidase: redox regulation and drug resistance.Advances in cancer research · 2014Review
- Early anti-oxidative and anti-proliferative curcumin effects on neuroglioma cells suggest therapeutic targets.Neurochemical research · 2008Article
- Butyrate reduces liver metastasis of rat colon carcinoma cells in vivo and resistance to oxidative stress in vitro.Clinical & experimental metastasis · 2004Article
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4 authors at 1 institution in 1 country.
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Abstract
Gamma glutamyltransferase (GGT) is a plasma membrane bound enzyme that initiates the degradation of glutathione. The presence of several promoters in the rat GGT gene indicates strict control and regulation of its expression. The aim of this study was to investigate whether the GGT gene was regulated differently after butyrate-induced differentiation and oxidative stress exposure of rat colon carcinoma cells and whether the regulation was related to the glutathione level. The activity of GGT was upregulated in a time-and-dose dependent manner after both butyrate and menadione incubations. The presence of antioxidants blocked the menadione but not the butyrate mediated induction of the enzyme. The level of intracellular glutathione was reduced after menadione, but not after butyrate incubations. Depletion of glutathione alone did not alter GGT activity. Reactive oxygen species (ROS) were not produced after incubations with butyrate, while menadione incubations produced ROS. The multiple GGT mRNA transcripts (mRNA I-V) that originate from the five distinct promoters were all present in the cell line. Incubations with butyrate enhanced mRNA II and IV transcripts whereas a reduction in mRNA IV-1 was noted during menadione incubations. The level of total GGT mRNA (I-V) was not altered when related to the amount of total beta-actin mRNA. We conclude that GGT activity can be upregulated by at least two distinct mechanisms during differentiation and oxidative stress. Apparently, the regulation of the enzyme is not directly linked to the intracellular level of glutathione.
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