Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Acimovic, J; Lövgren-Sandblom, A; Olin, M; Ali, Z; Heverin, M; Schüle, R; Schöls, L; Fischler, B; Fickert, P; Trauner, M; Björkhem, I.
Sulphatation does not appear to be a protective mechanism to prevent oxysterol accumulation in humans and mice.
PLoS One. 2013; 8(7):e68031-e68031
Doi: 10.1371/journal.pone.0068031
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- Co-Autor*innen der Med Uni Graz
- Fickert Peter
- Trauner Michael
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- Abstract:
- 24S- and 27-hydroxycholesterol (24OHC and 27OHC) are potent regulators of different biochemical systems in vitro and are the major circulating oxysterols. A small fraction of these oxysterols has been reported to be sulphated but there are no detailed studies. We considered the possibility that sulphatation is a protective mechanism preventing accumulation of free oxysterols. Using an accurate assay we found the sulphated fraction of 24OHC and 27OHC in circulation of adults to be less than 15% of total. In two patients with a mutation in CYP7B1 and markedly increased levels of 27OHC the sulphated fraction was 8% and 10% respectively. Infants with severe neonatal cholestasis had however markedly increased sulphate fraction of the above oxysterols. In untreated mice the degree of sulphatation of 24OHC and 27OHC in serum varied between 0 and 16%. Similar degree of sulphatation was found in two mouse models with markedly increased levels of 27OHC and 24OHC respectively. Bile duct ligated mice had higher levels of oxysterols than sham-operated controls but the sulphate fraction was not increased. We conclude that a primary increase in the levels of the oxysterols due to increased synthesis or reduced metabolism in adults and mice does not induce increased sulphatation.
- Find related publications in this database (using NLM MeSH Indexing)
- Adult -
- Aged -
- Animals -
- Cholesterol - blood
- Female -
- Humans -
- Hydroxycholesterols - blood
- Male -
- Mice -
- Middle Aged -
- Oxidation-Reduction -