By a News Reporter-Staff News Editor at Drug Week -- Research findings on Gastroenterology are discussed in a new report. According to news reporting from Copenhagen, Denmark, by NewsRx journalists, research stated, "Exposure to particles has been suggested to generate hepatosteatosis by oxidative stress mechanisms. We investigated lipid accumulation in cultured human hepatocytes (HepG2) and rat liver after exposure to four different carbon-based particles."
The news correspondents obtained a quote from the research from the University of Copenhagen, "HepG2 cells were exposed to particles for 3 h and subsequently incubated for another 18 h to manifest lipid accumulation. In an animal model of metabolic syndrome we investigated the association between intake of carbon black (CB, 14 nm) particles and hepatic lipid accumulation, inflammation and gene expression of Srebp-1, Fasn and Scd-1 involved in lipid synthesis. There was a concentration-dependent increase in intracellular lipid content after exposure to CB in HepG2 cells, which was only observed after co-exposure to oleic/palmitic acid. Similar results were observed in HepG2 cells after exposure to diesel exhaust particles, fullerenes C-60 or pristine single-walled carbon nanotubes. All four types of particles also generated oxidatively damaged DNA, assessed as formamidopyrimidine DNA glycosylase (FPG) sensitive sites, in HepG2 cells after 3 h exposure. The animal model of metabolic syndrome showed increased lipid load in the liver after one oral exposure to 6.4 mg/kg of CB in lean Zucker rats. This was not associated with increased iNOS staining in the liver, indicating that the oral CB exposure was associated with hepatic steatosis rather than steatohepatitis. The lipid accumulation did not seem to be related to increased lipogenesis because there were unaltered gene expression levels in both the HepG2 cells and rat livers."
According to the news reporters, the research concluded: "Collectively, exposure to particles is associated with oxidative stress and steatosis in hepatocytes."
For more information on this research see: Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles. Toxicology and Applied Pharmacology, 2014;274(2):350-360. Toxicology and Applied Pharmacology can be contacted at: Academic Press Inc Elsevier Science, 525 B St, Ste 1900, San Diego, CA 92101-4495, USA. (Elsevier - www.elsevier.com; Toxicology and Applied Pharmacology - www.elsevier.com/wps/product/cws_home/622951)
Our news journalists report that additional information may be obtained by contacting L.K. Vesterdal, University of Copenhagen, Environm Hlth Sect, Dept. of Public Hlth, DK-1014 Copenhagen K, Denmark. Additional authors for this research include P.H. Danielsen, J.K. Folkmann, L.F. Jespersen, K. Aguilar-Pelaez, M. Roursgaard, S. Loft and P. Moller (see also Gastroenterology).
Keywords for this news article include: Europe, Denmark, Copenhagen, Hepatocytes, DNA Research, Gastroenterology
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