The most frequent adverse effects of AFB1 in chicken are low performance, the depression of the immune system, and a reduced quality of both eggs and meat, leading to economic losses. Since oxidative stress plays a major role in AFB1 toxicity, natural products are increasingly being used as an alternative to mineral binders to tackle AFB1 toxicosis in farm animals. In this study, an in vivo trial was performed by exposing broilers for 10 days to AFB1 at dietary concentrations approaching the maximum limits set by the EU (0.02 mg/kg feed) in the presence or absence of turmeric powder (TP) (included in the feed at 400 mg/kg). The aims were to evaluate (i) the effects of AFB1 on lipid peroxidation, antioxidant parameters, histology, and the expression of drug transporters and biotransformation enzymes in the liver; (ii) the hepatic accumulation of AFB1 and its main metabolites (assessed using an in-house-validated HPLC-FLD method); (iii) the possible modulation of the above parameters elicited by TP. Broilers exposed to AFB1 alone displayed a significant increase in lipid peroxidation in the liver, which was completely reverted by the concomitant administration of TP. Although no changes in glutathione levels and antioxidant enzyme activities were detected in any treatment group, AFB1 significantly upregulated and downregulated the mRNA expression of CYP2A6 and Nrf2, respectively. TP counteracted such negative effects and increased the hepatic gene expression of selected antioxidant enzymes (i.e., CAT and SOD2) and drug transporters (i.e., ABCG2), which were further enhanced in combination with AFB1. Moreover, both AFB1 and TP increased the mRNA levels of ABCC2 and ABCG2 in the duodenum. The latter changes might be implicated in the decrease in hepatic AFB1 to undetectable levels (<LOD) in the TP supplemented group. Overall, our findings further support the use of TP as an effective feeding strategy to prevent AFB1-related adverse effects in broilers.

Aflatoxin B1 (AFB1) can impair the growth of chickens and reduce the quality of eggs and meat, resulting in significant economic losses. The inclusion of mycotoxin detoxifying agents (MyDA) with binding properties in the diet is an efficient tool to reduce their absorption rate in the gastrointestinal tract. Our aim was to investigate the ability of two innovative MyDA (SeOX, a feed additive featuring a tri-octahedral smectite mixed with lignocellulose, and CHS, a di-octahedral smectite functionalized with an organic non-toxic modifier) in both reducing the bio-accessibility and mitigating the adverse effects of AFB1 in broilers exposed for 10 days to concentrations approaching the European Union maximum limits in feed (0.02 mg/kg). The amount of AFB1 in the excreta of birds, collected over four consecutive days (starting on day 7), was significantly lower (p < 0.001) in the group exposed to AFB1 alone compared to the groups treated with either SeOX or CHS. The calculated bio-accessibility was decreased by nearly 30% with both MyDA. This positive effect was reflected by a significant reduction (p < 0.001) in the oxidative stress (measured as serum antioxidant capacity and hepatic lipid peroxidation) induced by AFB1. Although antioxidant enzyme activities and glutathione levels were unaffected by any treatment, AFB1 significantly induced (p < 0.001) the upregulation of CYP2A6 and the downregulation of Nrf2; the latter was reverted by each MyDA. Overall, these results demonstrate that the selected MyDA are effective in limiting the AFB1 absorption rate, thereby mitigating or even reverting the oxidative stress induced by AFB1 in broilers.

Ochratoxin A (OTA), Zearalenone (ZEA), and Fumonisins (FB) are common contaminants of poultry feed associated with oxidative damage and potentially dangerous residues in products from exposed animals. We investigated the molecular effects in broilers of a short-term (10 days) dietary exposure to OTA (0.26 mg/kg), ZEA (2.9 mg/kg), or FB (60 mg/kg) on cytochrome P450 enzymes (CYP), drug transporters (DT) and the antioxidant defence system. OTA markedly decreased serum antioxidant capacity, while all mycotoxins depressed reduced glutathione content and increased lipid peroxidation in the liver, indicating a hepatic pro-oxidant effect. All the tested mycotoxins also reduced both the activities and the gene expression of selected antioxidant enzymes in the liver and duodenum as a result of the modulation of the Nrf2/Keap1 pathway. Moreover, mycotoxins differentially altered the hepatic and intestinal gene expression of CYP enzymes (i.e., CYP2A6, CYP2C45, CYP3A4, and CYP1A isoforms). Finally, the transcription of selected DT (i.e., ABCB1, ABCC2 and ABCG2) was generally enhanced in both the liver and duodenum. In conclusion, short-term exposure to OTA, ZEA, or FB at dietary concentrations higher than those recommended in the EU, but occurring in third countries, not only disrupt the antioxidant defence but also affect the expression of CYP and DT, which might potentially alter the kinetics of drugs and toxicants. Our results provide new insights into mycotoxin adverse effects in the light to assess the effectiveness of new mitigation strategies that contribute to food and feed safety.