ArticleNaunyn-Schmiedeberg's archives of pharmacology2009
Ruthenium red protects HepG2 cells overexpressing CYP2E1 against acetaminophen cytotoxicity.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Hepatoselective Nitric Oxide (NO) Donors, V-PYRRO/NO and V-PROLI/NO, in Nonalcoholic Fatty Liver Disease: A Comparison of Antisteatotic Effects with the Biotransformation and Pharmacokinetics.Drug metabolism and disposition: the biological fate of chemicals · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied the mechanisms of acetaminophen (APAP) cytotoxicity in HepG2 cells overexpressing cytochrome p4502E1, particularly the role of oxidative/nitrosative stress and ryanodine Ca2+ channel. Cells were grown for 24 h with APAP in the presence or absence of 4-methylpyrazole (4MP), L-arginine methyl ester (L-NAME), superoxide dismutase (SOD), or ruthenium red (RuR). Drug cytotoxicity was also tested in cells pretreated overnight with V-PYRRO/NO. APAP was without effect on empty vector-transfected cells, but damaged CYP2E1-transfected cells and this was abolished by RuR, reduced by 4MP, or V-PYRRO/NO but affected by L-NAME or SOD. APAP increased microsomal [3H]-ryanodine binding, while microsomal Ca2+ uptake was significantly lowered. RuR increased net microsomal Ca2+ uptake and normalized cytosolic Ca2+ levels. We can conclude that neither oxidative nor nitrosative stress is relevant to APAP cytotoxicity in cultured HepG2 cells, but our results point to ryanodine receptors as a potential crucial protein in the early stages of APAP cytotoxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.