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Effect of fumonisin B1 on structure and function of macrophage plasma membrane
Maria C Ferrante1, Rosaria Meli, Giuseppina Mattace Raso
1Department of Pathology and Animal Health, University of Naples Federico II, Via Delpino 1, 80137, Naples, Italy.
Abstract:
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.
Insights
Fumonisin B1 (FB1) mycotoxin increases macrophage membrane fluidity and endocytosis while causing oxidative stress. Interferon-gamma (IFN-gamma) can reverse these harmful FB1 effects.
Area of Science:
- Toxicology
- Immunology
- Cell Biology
Background:
- Fumonisin B1 (FB1) is a mycotoxin from Fusarium fungi with known toxic effects.
- FB1 exhibits nephrotoxic, neurotoxic, hepatotoxic, carcinogenic, and immunosuppressive properties in humans and animals.
Purpose of the Study:
- To investigate FB1-induced modifications in plasma membrane fluidity, endocytosis, and peroxidative damage.
- To evaluate these effects in the macrophage cell line J774A.1.
Main Methods:
- Exposure of J774A.1 macrophages to varying concentrations of FB1 (1-10 microM).
- Measurement of membrane fluidity and horseradish peroxidase (HRP) endocytosis.
- Assessment of malondialdehyde (MDA) production as an indicator of peroxidative damage.
- Evaluation of the effect of Interferon-gamma (IFN-gamma) on FB1-induced changes.
Main Results:
- FB1 significantly enhanced macrophage membrane fluidity.
- FB1 increased HRP endocytosis in a time- and concentration-dependent manner, with significant effects at 10 microM.
- FB1 induced membrane peroxidative damage, evidenced by increased MDA production.
- IFN-gamma (100 U/ml) reverted the FB1-induced increase in HRP endocytosis.
Conclusions:
- FB1 alters macrophage plasma membrane properties, including fluidity and endocytosis.
- FB1 induces oxidative stress in macrophages through peroxidative damage.
- These findings offer insights into FB1's role in macrophage dysfunction and disease pathogenesis.