FUMONISIN B-1-INDUCED INCREASES IN NEUROTRANSMITTER METABOLITE LEVELSIN DIFFERENT BRAIN-REGIONS OF BALB C MICE/

Fumonisin B-1 a toxin produced by Fusarium moniliforme, causes a varie ty of diseases in animals, including those involving the central nervo us system, such as equine leukoencephalomalacia; (ELEM). The changes o f biogenic amines may reflect fumonisin B-1 neurotoxicity. It was prev iously reported that consumption of feed contaminated with Fusarium mo niliforme cultures produced an elevation of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of 5-hydroxytryptamine (5-HT), in whol e rat brains. In a subsequent study from the same laboratory, rats giv en fumonisin B-1 orally for 4 weeks showed no changes in neurotransmit ter levels of the whole brain. In the current study, groups of five ma le BALB/c mice were injected with fumonisin B-1 subcutaneously at dose s of 0, 0.25, 0.75, 2.25, 6.75 mg kg(-1) body weight daily for 5 days. One day after the last treatment, their brains were dissected into ce rebrum, cerebellum, medulla oblongata, midbrain, corpus striatum and h ypothalamus. Levels of norepinephrine (NE), dopamine (DA), DA metaboli tes, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), a nd 5-HT and 5-HIAA were determined. A significant elevation of HVA was observed in mice treated with high doses of fumonisin B-1 in most bra in regions. In striatum, a decrease of 5-HT was observed by the fumoni sin B-1, treatment. Ratios of neurotransmitters to metabolites such as HVA/DA and 5-HIAA/5-HT were elevated in several brain regions of the treated groups. An accumulation of neurotransmitter metabolites is sug gestive of increased neuronal activity,or interference with their effl ux from cells. (C) 1998 Elsevier Science Inc. All rights reserved.