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Fumonisin B1-induced increases in neurotransmitter metabolite levels in different brain regions of BALB/c mice.
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998 Oct; 120(3):457-65.CB

Abstract

Fumonisin B1, a toxin produced by Fusarium moniliforme, causes a variety of diseases in animals, including those involving the central nervous system, such as equine leukoencephalomalacia (ELEM). The changes of biogenic amines may reflect fumonisin B1 neurotoxicity. It was previously reported that consumption of feed contaminated with Fusarium moniliforme cultures produced an elevation of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of 5-hydroxytryptamine (5-HT), in whole rat brains. In a subsequent study from the same laboratory, rats given fumonisin B1 orally for 4 weeks showed no changes in neurotransmitter levels of the whole brain. In the current study, groups of five male BALB/c mice were injected with fumonisin B1 subcutaneously at doses 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 cerebrum, cerebellum, medulla oblongata, midbrain, corpus striatum and hypothalamus. Levels of norepinephrine (NE), dopamine (DA), DA metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and 5-HT and 5-HIAA were determined. A significant elevation of HVA was observed in mice treated with high doses of fumonisin B1 in most brain regions. In striatum, a decrease of 5-HT was observed by the fumonisin B1 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 suggestive of increased neuronal activity or interference with their efflux from cells.

Authors+Show Affiliations

Tsunoda M
Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens 30602-7389, USA.
Dugyala RR
No affiliation info available
Sharma RP
No affiliation info available

MeSH

3,4-Dihydroxyphenylacetic AcidAnimalsBrainBrain ChemistryCarboxylic AcidsCarcinogens, EnvironmentalDopamineFumonisinsHomovanillic AcidHydroxyindoleacetic AcidInjections, SubcutaneousMaleMiceMice, Inbred BALB CNeurotransmitter AgentsNorepinephrineSerotonin

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9827064

Citation

Tsunoda, M, et al. "Fumonisin B1-induced Increases in Neurotransmitter Metabolite Levels in Different Brain Regions of BALB/c Mice." Comparative Biochemistry and Physiology. Part C, Pharmacology, Toxicology & Endocrinology, vol. 120, no. 3, 1998, pp. 457-65.
Tsunoda M, Dugyala RR, Sharma RP. Fumonisin B1-induced increases in neurotransmitter metabolite levels in different brain regions of BALB/c mice. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998;120(3):457-65.
Tsunoda, M., Dugyala, R. R., & Sharma, R. P. (1998). Fumonisin B1-induced increases in neurotransmitter metabolite levels in different brain regions of BALB/c mice. Comparative Biochemistry and Physiology. Part C, Pharmacology, Toxicology & Endocrinology, 120(3), 457-65.
Tsunoda M, Dugyala RR, Sharma RP. Fumonisin B1-induced Increases in Neurotransmitter Metabolite Levels in Different Brain Regions of BALB/c Mice. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998;120(3):457-65. PubMed PMID: 9827064.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fumonisin B1-induced increases in neurotransmitter metabolite levels in different brain regions of BALB/c mice. AU - Tsunoda,M, AU - Dugyala,R R, AU - Sharma,R P, PY - 1998/11/25/pubmed PY - 1998/11/25/medline PY - 1998/11/25/entrez SP - 457 EP - 65 JF - Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology JO - Comp Biochem Physiol C Pharmacol Toxicol Endocrinol VL - 120 IS - 3 N2 - Fumonisin B1, a toxin produced by Fusarium moniliforme, causes a variety of diseases in animals, including those involving the central nervous system, such as equine leukoencephalomalacia (ELEM). The changes of biogenic amines may reflect fumonisin B1 neurotoxicity. It was previously reported that consumption of feed contaminated with Fusarium moniliforme cultures produced an elevation of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of 5-hydroxytryptamine (5-HT), in whole rat brains. In a subsequent study from the same laboratory, rats given fumonisin B1 orally for 4 weeks showed no changes in neurotransmitter levels of the whole brain. In the current study, groups of five male BALB/c mice were injected with fumonisin B1 subcutaneously at doses 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 cerebrum, cerebellum, medulla oblongata, midbrain, corpus striatum and hypothalamus. Levels of norepinephrine (NE), dopamine (DA), DA metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and 5-HT and 5-HIAA were determined. A significant elevation of HVA was observed in mice treated with high doses of fumonisin B1 in most brain regions. In striatum, a decrease of 5-HT was observed by the fumonisin B1 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 suggestive of increased neuronal activity or interference with their efflux from cells. SN - 1367-8280 UR - https://www.unboundmedicine.com/medline/citation/9827064/Fumonisin_B1_induced_increases_in_neurotransmitter_metabolite_levels_in_different_brain_regions_of_BALB/c_mice_ L2 - https://antibodies.cancer.gov/detail/CPTC-MS4A1-1 DB - PRIME DP - Unbound Medicine ER -