Interaction of aflatoxin B₁ and fumonisin B₁ in mice causes immunotoxicity and oxidative stress: Possible protective role using lactic acid bacteria

摘要

Abstract Aflatoxins (AF) are important foodborne mycotoxins implicated in human health and have immunocytotoxic effects. The aims of this study were to evaluate a new aflatoxin B₁ (AFB₁) and fumonisin B₁ (FB₁)-binding/degrading micro-organism for biological detoxification, to examine its ability to degrade AFB₁ and FB₁ in liquid medium, and to evaluate its potential in vivo protective role against any combined effects from AFB₁ and FB₁ on host splenocyte caspase-3 activity (reflecting DNA damage/cell death) and mRNA levels of select inflammation-regulating cytokines. Balb/c mice were divided into groups (10/group) and treated daily for 2 weeks by oral gavage with AFB₁ (80?μg/kg BW), FB₁ (100?μg/kg), AFB₁?+?FB₁, or lactic acid bacteria (Lactobacillus paracasei BEJ01, 2?×?109?CFU/L, ～2?mg/kg) – alone or in combination with the AFB₁ and/or FB₁. After the exposures, spleens were collected for measures of caspase-3 activity, lipid peroxidation (LP), and glutathione (GSH) content, expression of anti-oxidation protective enzymes (GPx and SOD), and mRNA levels of inflammation-regulating cytokines (e.g. IL-10, IL-4, IFNγ, TNFα). Thymii were also removed for analysis of apoptosis. The results indicated that, in the spleen, exposure to the mycotoxins led to increased caspase-3 activity, LP, and IL-10 and IL-4 mRNA levels, but decreased GSH content and down-regulated expression of GPx and SOD, and of IFNγ and TNFα mRNA. Co-treatment using Lactic Acid Bacteria (LAB) with AFB₁ or FB₁ suppressed levels of DNA fragmentation, normalized splenic LP and increased GSH levels, up-regulated expression of GPx and SOD, and normalized mRNA levels of the analyzed cytokines. It is concluded that AFB₁ and FB₁ might have combinational (synergistic moreso than additive) toxic effects in situ. Further, it can be seen that use of LAB induced protective effects against the oxidative stress and (immuno)toxicity of these agents in part through adhesion (and so likely diminished bioavalability).