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Issue title: The Third Conference of the International CoQ10 Association
Article type: Research Article
Authors: Dallner, Gustav | Brismar, Kerstin | Chojnacki, Tadeusz | Swiezewska, Ewa
Affiliations: Department of Biochemistry and Biophysics, Stockholm University, 106 91 Stockholm, Sweden | Department of Molecular Medicine, Karolinska Hospital, 171 76 Stockholm, Sweden | Institute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-532 Warsaw, Poland
Note: [] Corresponding author: Tel.: +46 8 674 78 26; Fax: +46 8 15 36 79; E-mail: gustav@dbb.su.se
Abstract: All animal cells synthesize sufficient amounts of coenzyme Q (CoQ) and the cells also possess the capacity to metabolize the lipid. The main product of the metabolism is an intact ring with a short carboxylated side chain which glucuronidated in the liver and excreted mainly into the bile (Nakamura et al., Biofactors 9 (1999), 111–119). In other cells CoQ is phosphorylated, transferred into the blood and excreted through the urine. The biosynthesis of this lipid is regulated by nuclear receptors. PPARα is not required for the biosynthesis, or induction upon cold exposure, but it is necessary for the elevated CoQ synthesis during peroxisomal induction. RXRα is involved in the basal synthesis of CoQ and also in the increased synthesis upon cold treatment but is not required for peroxisomal induction. Dietary CoQ in human appear in the blood and it is taken up by mononuclear but not polynuclear cells. The former cells display a specific phospholipid modification, an increase of arachidonic acid content. In monocytes the CoQ administration leads to a significant decrease of the β2-integrin CD11b and the complement receptor CD35. CD11b is one of the adhesion factors regulating the entry of these cells into the arterial wall which demonstrates that the anti-atherogenic effect of CoQ is mediated by other mechanisms beside its antioxidant protection.
Keywords: Coenzyme Q metabolism, conjugation of metabolites, nuclear receptors, monocytes, β2-integrins, atherosclerosis
Journal: BioFactors, vol. 18, no. 1-4, pp. 11-22, 2003
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