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EFFECT OF FUMONISIN B1 ON STRUCTURE AND FUNCTION OF MACROPHAGE PLASMA MEMBRANE
Fumonisin B1 (FB1), a mycotoxin produced by Fusarium moniliforme and related fungi, is nephrotoxic, neurotoxic, hepatotoxic, carcinogenic and immunosuppressive in animals and man. In this study we evaluate the modifications of fluidity, endocytosis and peroxidative damage of plasma membrane induced by FB1 in macrophage cell line J774A.1. In these immune cells FB1 (1-10 microM) enhances membrane fluidity and increases, time-dependently, the horseradish peroxidase (HRP) endocytosis. This effect is concentration-dependent, significant at 10 microM, and reverted by IFN-gamma (100 U/ml). Moreover, FB1 (1-10 microM) induces a membrane peroxidative damage as evident by the increase of malondialdehyde (MDA) production. All these mycotoxin effects provide additional insight into potential mechanism by which FB1, in macrophages, might enhance membrane damage and oxidative stress contributing to the pathogenesis of mycotoxin induced diseases
Inhibition of inducible nitric oxide synthase and cyclooxygenase-2 expression by flavonoids in macrophage J774A.1.
Effects of fenvalerate on membrane fluidity in the cerebellum and cerebral cortex of rats.
Effects of fenvalerate on membrane fluidity in the cerebellum and cerebral cortex of rats.
Effects of fenvalerate on membrane in fluidity in the cerebellum and cerebral cortex of rats
The effects of fenvalerate on rat cerebral cortex and cerebellum cell membrane fluidity were investigated using a fluorescence polarization technique. The study was performed in vitro and in vivo, producing different data according to the experimental conditions. In vitro, fenvalerate induced a significant concentration-dependent increase in membrane fluidity in both brain regions; in vivo the authors observed that membrane fluidity increased in a dose and time dependent manner in the cerebellum cells of rats treated with fenvalerate for 2, 5 or 30 days, whilst no change was found in cerebral cortex cells. This latter result could be explained by the increasing accumulation of fenvalerate and its metabolites in the cerebellum where the levels of conjugation activity appear to be very low
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