Food products are susceptible to contamination by mycotoxins, and aflatoxin B1 (AFB1) stands as the most toxic among them. AFB1 intoxication results in distinct signs, including widespread systemic toxicity. Aspartame (ASP) is an artificial sweetener used as a sugar substitute in many products, and compelling evidence indicates ASP can be toxic. Interestingly, mechanisms underlying ASP and AFB1 toxicity involve oxidative stress. In this context, concomitant use of ASP and AFB1 in a meal may predispose to currently unidentified behavioural and biochemical changes. Therefore, we evaluated the effect of AFB1 (250 μg/kg, intragastrically (i.g.)) and/or ASP (75 mg/kg, i.g.) exposure for 7 days on behavioural and biochemical markers of oxidative stress in male Wistar rats. AFB1 and/or ASP increased hepatic glutathione S-transferase (GST) activity when compared to controls. In the kidneys, increased GST activity was detected in AFB1 and AFB1+ASP groups. In addition, AFB1 and or ASP elicited behavioural changes in the open field, marble burying and splash tests, however no additive effects were detected. Altogether, present data suggest AFB1 and ASP predispose to anxiety- and obsessive-compulsive-like symptoms, as well as to enzymatic defence system imbalance in liver and kidney of Wistar rats.

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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.