Water-soluble pristine C60 fullerene attenuates acetaminophen-induced liver injury

Autor:	Uwe Ritter, Yuriy Prylutskyy, Natalia Dziubenko, Volodymyr Rybalchenko, Tetyana S Herheliuk, O.V. Lynchak, H.M. Kuznietsova
Rok vydání:	2019
Předmět:	Medicine (General) QH301-705.5 Bilirubin Pharmaceutical Science 02 engineering and technology Pharmacology medicine.disease_cause General Biochemistry Genetics and Molecular Biology hepg2 cells 03 medical and health sciences chemistry.chemical_compound R5-920 Blood serum Medicine Biology (General) Original Research 030304 developmental biology Liver injury Hepatitis 0303 health sciences Creatinine business.industry c60 fullerene General Medicine acetaminophen-induced liver injury 021001 nanoscience & nanotechnology medicine.disease Free radical scavenger Acetaminophen chemistry egfr 0210 nano-technology business Oxidative stress medicine.drug
Zdroj:	BioImpacts, Vol 9, Iss 4, Pp 227-237 (2019) BioImpacts : BI
ISSN:	2228-5652 2228-5660
DOI:	10.15171/bi.2019.28
Popis:	Introduction: Oxidative stress has been suggested as the main trigger and pathological mechanism of toxic liver injury. Effects of powerful free radical scavenger С60 fullerene on rat liver injury and liver cells (HepG2 line) were aimed to be discovered.Methods: Acute liver injury (ALI) was simulated by single acetaminophen (APAP, 1000 mg/kg) administration, on a chronic CLI, by 4 weekly APAP administrations. Pristine C60 fullerene aqueous colloid solution (C60FAS; initial concentration 0.15 mg/mL) was administered per os or intraperitoneally at a dose of 0.5 mg/kg (ALI) or 0.25 mg/kg (CLI) daily for 2 or 28 days, respectively, after first APAP dose. Animals were sacrificed at 24th hour after the last dose. Biochemical markers of blood serum and liver autopsies were analyzed. EGFR expression in HepG2 cells after 48-hour incubation with C60FAS was assessed. Results: Increase of serum conjugated and unconjugated bilirubin (up to 1.4-3.7 times), ALT (by 31-37%), and AST (by 18%) in non-treated ALI and CLI rats were observed, suggesting the hepatitis (confirmed by histological analysis). Liver morphological state (ALI, CLI), ALT (ALI and CLI), bilirubin (CLI), α-amylase, and creatinine (ALI) were normalized with C60FAS administration in both ways, which may indicate its protective impact on liver. However, unconjugated bilirubin sharply increased in ALI animals receiving C60FAS (up to 12 times compared to control), suggesting the augmentation of bilirubin metabolism. Furthermore, C60FAS inhibited EGFR expression in HepG2 cells in a dose-dependent manner. Conclusion: C60FAS could partially correct acute and chronic toxic liver injury, however, it could not normalize bilirubin metabolism after acute exposure.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b95ae74f285707fb1b87b9dd800feeb2 https://doi.org/10.15171/bi.2019.28 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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