Lycopene mitigates T-2 toxin-induced systemic inflammation and oxidative stress in association with gut microbiota...

T-2 toxin is a trichothecene mycotoxin produced by Fusarium species and can cause disease after contaminated food or feed ingestion. This study aimed to investigate the impact of lycopene (Ly) on systemic inflammation, oxidative stress, and dysbiosis in mice exposed to T-2 toxin. A total of 20 male BALB/c mice (6 weeks old, weighing 23.5 ± 0.32 g) randomly divided into four groups (n = 5): Control (Cont), Ly, T-2, and T-2 + Ly groups. Findings revealed that Ly enhanced the body weight, feedd, and water intake that have been reduced by T-2. Ly increased the villus height (VH) and VH: crypt depth (CD) and decreased CD and villus width (VW) in ileum compared to the T-2 group. In alpha diversity, Staphylococcus and Corynebacterium were the most prevalent in Cont group; Staphylococcus, and Lactobacillus, were the most prevalent in T-2 group; Candidatus-Arthromitus and Staphylococcus were the most prevalent in T-2 + Ly group. Moreover, T-2 mice had significantly (p < 0.05) greater levels of interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), Interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) than Cont, while the Ly significantly (p < 0.05) lowered their concentration. The T-2 mice had significantly (p < 0.05) higher levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while their catalase (CAT),, glutathione (GSH), adenosine triphosphate (ATP), and superoxide dismutase 1(SOD1) activities were significantly (p < 0.05) lower than Cont. Ly significantly (p < 0.05) restored their concentration. Moreover, there was a significant reduction (p < 0.05) of hexanoic, butyric, acetic, pentanoic, and Heptanoic acids in the T-2 mice compared to Cont. In contrast, treatment with Ly was found to significantly restore their levels compared to T-2 group. We conclude that Ly administration in the context of T-2-induced toxicity may help attenuate systemic oxidative stress and inflammation, possibly through modulation of gut microbiota and fecal short-chain fatty acids (SCFAs).