Avaliação de efeitos comportamentais e bioquímicos induzidos pela exposição à fumonisina B1 em camundongos

Abstract

Fumonisins are mycotoxins produced by several species of fungi belonging to the genus Fusarium, especially by Fusarium verticillioides. Among the various fumonisins, fumonisin B1 (FB1) is the one with the highest incidence and also considered to be the most toxic. This mycotoxin occurs as a natural contaminant in several agricultural products, mainly in corn, and consequently in products derived from it. Contamination of humans and animals by this mycotoxin can occur directly, through the ingestion of contaminated cereals, or indirectly, by the ingestion of contaminated products. FB1 is related with the occurrence of various damages to human and animal health, such as neurological, immunological, nephrotoxicity and hepatotoxicity, among others. Mechanism by FB1 toxicity is not completely elucidated, but the main mechanism is believed to be the alteration of the metabolism of the sphingolipids. In addition, we have been investigating the relation of FB1 with imbalance in the oxidative system of the organism as a possible mechanism of its toxicity.Thus, the objective of this study is to evaluate the toxic effects caused by the intraperitoneal administration of FB1 (8mg/kg b.w.) for four days, on behavioral parameters and oxidative stress in young male mice. After the four doses, the animals were submitted to behavioral tests (open field, object recognition, Marble Buryng, nest building) and then the biochemical analyzes were performed. The only behavioral effect observed was the increase in the nest test score after treatment with FB1. In liver, kidney and lung, the non-enzymatic oxidative stress markers analyzed were: thiobarbituric acid reactive species (TBARS), non-protein thiol content (NPSH), ascorbic acid content, antioxidant power by the iron reduction method (FRAP) and determination of indirect nitric oxide (NOx). In the cerebral cortex and hippocampus samples, the content of non-protein thiols (NPSH) and the antioxidant power by the iron reduction method (FRAP) and changes in the immunoreactivity of protein kinase C (PKC-Ser957) in the hippocampus. The results show that FB1 promotes changes in oxidative stress parameters differently from those of the organ, as observed by the increase of NPSH in liver and lung and decrease of FRAP in liver and kidney. At the brain level, no change was observed in markers of oxidative stress in the cortex and hippocampus, as well as no change in the immunoreactivity of protein kinase C in the hippocampus. It can be concluded that the administration of FB1 altered oxidative parameters in liver, kidney and lung and predisposed changes in the parameters related to the anxiety of the animals.