Objectives: Aflatoxin B1 (AFB1) is the most widespread mycotoxin, and it is a feed contaminant and is highly toxic, causing carcinogenic, mutagenic, and teratogenic effects. Many researches clarified the peripheral effects of the exposition to AFB1; however, there are few studies explaining their effects on central nervous system. The aim of the present study was to evaluate the effects caused by acute oral administration of AFB1 on behavioral tests and selected biochemical parameters. Methods: Young male Wistar rats received a single administration of AFB1 (250 µg/kg/i.g.) and 48 hours thereafter they were subjected to behavioral analysis. After the tests, biochemical parameters were measured in the cerebral cortex. Results: Acute treatment with AFB1 caused neurotoxic effects, evidenced by a significant reduction in the levels of non-enzymatic antioxidant defenses, ascorbic acid, and non-protein sulfhydryl groups. In addition, AFB1 increased protein kinase C (PKC) activation, evidenced by an increase in phosphorylation of Ser⁹⁵⁷ of PKCα. Discussion: In this acute protocol, a single oral administration of AFB1 was able to cause changes in important neurochemical parameters, without concomitant, detectable behavioral alterations. These results reinforce that monitoring mycotoxin levels in food is essential to guarantee food security.

Aflatoxin B₁ (AFB₁) is the most common toxic mycotoxin that contaminates food. The treatment of its intoxication and the management of contaminations are a constant subject of health agendas worldwide. However, such efforts are not always enough to avoid population intoxication. Our objective was to investigate whether intermittent exposure to AFB₁ would cause any impairment in biochemical and behavioral parameters, intending to simulate an irregular consumption. Male Wistar rats received four AFB₁ administrations (250 μg/kg) by intragastric route separated by a 96-h interval. Toxicity was evaluated using behavioral tests (open field, object recognition, nest construction, marble burying, and splash test), biochemical markers of oxidative stress (cerebral cortex, hippocampus, liver, and kidneys), and plasma parameters of hepatic and renal functions. The intermittent exposure caused no modification in body weight gain as well as in organ weight. Both control and AFB₁ groups presented similar profiles of behavior to all tests performed. Furthermore, AFB₁ administrations alter neither antioxidant defenses nor markers of oxidation in all assayed tissues and in the plasma markers of hepatic and renal functions. Therefore, AFB₁ intermittent administration did not cause its common damage from exposure to this toxicant, which must be avoided, and additional studies are required.

The potential interactions among food additives/contaminants and the consequences to biological systems is a topic that is rarely addressed in scientific literature. Thus, the current study investigated if the combined administration of ASP and AFB₁ would impair hepatic and renal oxidative status. Male Wistar rats received during 14 days once a day ASP (75 mg/Kg) and/or AFB₁ (250 µg/Kg) through intragastric route. At the end of experimental protocol, samples of liver and kidneys were collected for assessing biochemical markers of oxidative status. In the hepatic tissue, the treatment with a single substance (ASP or AFB₁) caused an increase in TBARS levels, and a reduction in non-enzymatic antioxidant defenses (Vit C and NPSH levels and FRAP test). In the kidneys, TBARS levels were increased only in the group that received ASP + AFB₁. The association reduced NPSH content, while the treatment with AFB₁ reduced the FRAP levels. GST and CAT activities were increased in all treatments. Overall, ASP and AFB1 association presented higher toxic effects to the tissues. To the best of our knowledge, this is the first study demonstrating that the associated use of both ASP and AFB1 induces more extensive injuries in comparison to the effects caused by each one alone. Therefore, these data demonstrated that concomitant exposure to ASP and AFB₁ potentiated their oxidative damage in hepatic tissue, suggesting that this organ is particularly sensitive to the toxic action induced by these substances.