NDLI: Acetaminophen-induced S-nitrosylation and S-sulfenylation signalling in 3D cultured hepatocarcinoma cell spheroids

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Toxicology Research Vol - 5 Issue - 2

Toxicology Research Vol - 5 Issue - 1

Toxicology Research Vol -4

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

Acetaminophen-induced S-nitrosylation and S-sulfenylation signalling in 3D cultured hepatocarcinoma cell spheroids

Content Provider	Royal Society of Chemistry (RSC)
Author	Wrzesinski, Krzysztof Wojdyla, Katarzyna Fey, Stephen J. Williamson, James Rogowska-Wrzesinska, Adelina
Copyright Year	2016
Abstract	Acetaminophen (APAP) is possibly the most widely used medication globally and yet little is known of its molecular effects at therapeutic doses. Using a novel approach, we have analysed the redox proteome of the hepatocellular cell line HepG2/C3A treated with therapeutic doses of APAP and quantitated both individual protein abundance and their reversible S-nitrosylation (SNO) and S-sulfenylation (SOH) modifications by mass spectrometry. APAP treatment results in a late, transient increase in ATP production and a multiplicity of alterations in protein abundance and modifications. The majority of the differentially SNO or SOH modified proteins are found in the endoplasmic reticulum and cytosol, suggesting that the source of reactive species is there. The cellular response indicates: constraint of fatty acid metabolism; reduction in ribosome construction and protein synthesis (to conserve ATP); maintenance of glutathione levels (by increased synthetic capacity); and an increased NADPH production (via the pentose phosphate pathway). This response appears to be coordinated, directly or indirectly, by the canonical Wnt and Nrf2 signalling pathways. Combined with the known role of NAPQI, these studies suggest that the physiological and toxicological responses form a continuum: therapeutic doses of APAP produce reactive species and NAPQI in the cytoplasm but result in little permanent damage. The cell mounts a multifaceted response which minimises disruption and repairs are effected within a day or two. Higher doses of APAP lead to intensified reactive species production, which increasingly disturbs mitochondrial function and eventually leads to cell death.
Starting Page	905
Ending Page	920
Page Count	16
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	5
Issue Number	3
Journal	Toxicology Research
DOI	10.1039/c5tx00469a
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	APAP Phosphorylation Wnt signaling pathway Redox Proteome Metabolism Cytosol Protein Paracetamol Fatty acid Pentose The Cell Nicotinamide adenine dinucleotide NAPQI ATP Mass spectrometry Endoplasmic reticulum Adenosine triphosphate Cytoplasm Glutathione NFE2L2
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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Acetaminophen-induced S-nitrosylation and S-sulfenylation signalling in 3 D cultured hepatocarcinoma cell spheroids †

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