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Neurotransmitters in rats fed fumonisin B1
J K Porter1, K A Voss, W J Chamberlain
1Toxicology and Mycotoxin Research Unit, R. B. Russell Agriculture Research Center, USDA, ARS, Athens, Georgia 30613.
Summary
Fumonisin B1, a mycotoxin, did not alter key brain chemicals like serotonin in rats. However, high doses may disrupt norepinephrine and dopamine balance, suggesting other toxins from Fusarium moniliforme might cause neurotoxic effects.
Area of Science:
- Toxicology
- Neuroscience
- Mycology
Background:
- Fusarium moniliforme produces fumonisin B1, linked to equine leukoencephlomalacia.
- Previous studies indicated F. moniliforme toxins alter rat brain 5-hydroxyindoleacetic acid (5HIAA) and serotonin (5HT) levels.
- The neurochemical impact of isolated fumonisin B1 requires further investigation.
Purpose of the Study:
- To investigate the neurochemical effects of fumonisin B1 on rat brain and pineal gland.
- To determine if fumonisin B1 alone replicates the 5HIAA and 5HT imbalances observed with F. moniliforme exposure.
- To assess potential sex-based differences in neurochemical responses to fumonisin B1.
Main Methods:
- Male and female rats were administered fumonisin B1 at 15, 50, and 150 ppm for four weeks.
- Brain and pineal gland tissue concentrations of norepinephrine, dopamine, and serotonin metabolites (5HIAA, 5HT) were analyzed.
- Ratios including 5HIAA:5HT and norepinephrine:dopamine were calculated and compared.
Main Results:
- No significant changes were observed in brain 5HT, 5HIAA, or their ratios in rats treated with fumonisin B1.
- A decrease in the norepinephrine to dopamine ratio was noted in male rats receiving 150 ppm of fumonisin B1.
- No significant alterations in pineal gland neurochemical levels were detected.
Conclusions:
- Fumonisin B1 alone does not appear to cause the previously observed 5HT and 5HIAA imbalances in rat brains.
- A potential disruption of brain norepinephrine and dopamine systems may occur at high fumonisin B1 doses.
- Other mycotoxins produced by Fusarium moniliforme may be responsible for the neurotoxic effects associated with equine leukoencephlomalacia.

