CERAMIDE AND SPHINGOMYELIN LEVELS IN THE RAT BRAIN AFTER CHRYSIN INTAKE
HALINA CAR 1,4#, ANNA FIEDOROWICZ 1,2#, MAŁGORZATA ŻENDZIAN-PIOTROWSKA 3, ADRIAN CHABOWSKI 4, SYLWIA K. NALIWAJKO 5, KATARZYNA SOCHA 5, RENATA MARKIEWICZ-ŻUKOWSKA 5, WIOLETA J. OMELJANIUK 5, MARIA H. BORAWSKA 5*
1.Department of Experimental Pharmacology, Medical University of Bialystok, Poland
2.Laboratory of Tumor Molecular Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland
3.Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, Poland
4.Department of Physiology, Medical University of Bialystok, Poland
5.Department of Bromatology, Medical University of Bialystok, Poland
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The pathway of sphingolipid biosynthesis is important in intracellular communication and can be involved in oxidative stress reactions. Natural flavonoids, such as chrysin, present a wide range of antioxidative activities and their ingestion can have many beneficial effects. We studied the levels of ceramides (Cers) and sphingomyelin (SM) in rat brain after 7-day oral administration of chrysin at different doses. Cers and SM lipid fractions containing fatty acids of different chain length and saturation degree were separated by thin-layer chromatography (TLC) and analyzed using gas-liquid chromatography (GLC) technique. We observed the significant changes in the sphingolipid (SF) profiles. Chrysin intake decreased concentrations of Cers containing saturated (SAFA, Cer-C14:0, 16:0, 18:0, 24:0), monounsaturated (MUFA, Cer-C16:1, 24:1) and polyunsaturated fatty acids (PUFA), principally Cer-C18:2, 18:3, 20:4. The levels of SM-SAFA (SM-C14:0, 18:0), -MUFA (SM-C18:1) and -PUFA (SM-C18:2, 20:4, 22:6) were also reduced after the administration of chrysin. We suggest that the decrease in cerebral SF content may be involved in the antioxidative activities of chrysin. The substantial reduction of multiple Cer species levels in the brain may result in diminishing the potential Cers-dependent oxidative stress.
