دورية أكاديمية

Elevated citrate levels in non-alcoholic fatty liver disease: The potential of citrate to promote radical production

التفاصيل البيبلوغرافية
العنوان: Elevated citrate levels in non-alcoholic fatty liver disease: The potential of citrate to promote radical production
المؤلفون: van de Wier, B., Balk, J.M., Haenen, G.R.M.M., Giamouridis, D., Bakker, J.A., Bast, B.C., den Hartog, G.J.M., Koek, G.H., Bast, A.
المصدر: van de Wier , B , Balk , J M , Haenen , G R M M , Giamouridis , D , Bakker , J A , Bast , B C , den Hartog , G J M , Koek , G H & Bast , A 2013 , ' Elevated citrate levels in non-alcoholic fatty liver disease: The potential of citrate to promote radical production ' , Febs Letters , vol. 587 , no. 15 , pp. 2461-2466 . https://doi.org/10.1016/j.febslet.2013.06.019Test
سنة النشر: 2013
المجموعة: Maastricht University Research Publications
مصطلحات موضوعية: Citrate, Non-alcoholic fatty liver disease, Oxidative stress, Fenton reaction, Hydroxyl radical, Iron, MICROSOMAL LIPID-PEROXIDATION, HYDROXYL RADICALS, IRON CHELATORS, CITRIC-ACID, STEATOHEPATITIS, COMPLEXES, FERRITIN, DAMAGE
الوصف: Plasma citrate levels were found to be elevated in non-alcoholic fatty liver disease (NAFLD) patients. Cellular experiments indicated that increased citrate levels might originate from an excess of fatty acids. The impact of elevated citrate levels on oxidative stress was examined. It was found that citrate stimulated hydrogen peroxide induced intracellular oxidative stress in HepG2 cells. This was related to the promotion of iron mediated hydroxyl radical formation from hydrogen peroxide by citrate. The stimulating effect of citrate on the reactivity of iron promotes oxidative stress, a crucial process in the progression of NAFLD.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1016/j.febslet.2013.06.019
الإتاحة: https://doi.org/10.1016/j.febslet.2013.06.019Test
https://cris.maastrichtuniversity.nl/en/publications/cab0a81e-c991-4140-9319-df19e1ba1c07Test
حقوق: info:eu-repo/semantics/closedAccess
رقم الانضمام: edsbas.E107CED7
قاعدة البيانات: BASE