Journal
NUTRITIONAL NEUROSCIENCE
Volume 25, Issue 5, Pages 1056-1065Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/1028415X.2020.1833581
Keywords
fumonisins; myenteric plexus; NADH-diaphorase; NADPH-diaphorase; mitochondrial dysfunction; neuroplasticity; neurotoxicity
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This study found that diets containing fumonisins had no significant effects on food consumption or body weight in rats, but it did decrease the metabolic activity of myenteric neurons and nitrergic neurons. This decrease in metabolic activity had a negative impact on neuroplasticity of the enteric nervous system.
Fumonisins are naturally occurring mycotoxins that contaminate food for human and animal consumption. They have neurotoxic effects, but the mechanisms by which these toxins affect the nervous system are not fully known. In the present study, male Wistar rats were fed between 21 and 63 days of age with diets that contained fumonisins B-1+B-2 at 0, 1, and 4 mg/kg. The following variables were assessed: food consumption, growth, body weight gain, and blood parameters. Morphoquantitave analyses of the most metabolically active myenteric neurons were performed, detected by NADH-diaphorase activity. Nitrergic neurons were detected by NADPH-diaphorase activity. The fumonisin-containing diets did not significantly alter food consumption or the body or plasma parameters. These diets decreased the metabolic activity of jejunal myenteric neurons, reducing neuronal density of the most metabolic active neurons by 30.8% and the cell body area by 4.3%. The diets also decreased the cell body area of nitrergic neurons by 22.1%. The effects of fumonisin B-1 on the respiratory metabolism of isolated mitochondria in the brain and liver were also assessed. A decrease in oxygen consumption up to a 29% in the brain and 38% in the liver was observed in mitochondrial isolates to which 50 mu M fumonisin B-1 was added. The decrease in respiratory activity that was triggered by exposure to fumonisins was related to the lower metabolic activity of myenteric neurons, which had a negative impact on neuroplasticity of the enteric nervous system.
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