Aflatoxin B₁ (AFB₁) is a common mycotoxin contaminant in cereals that causes severe economic losses and serious risks to the health of humans and animals. In this paper, we investigated the characteristics of AFB₁ degradation by black soldier fly larvae (BSFL) combined with commensal intestinal microorganisms. Germ-free BSFL and non-sterile BSFL were reared on peanut meal spiked with AFB₁ for 10 days. The result showed that germ-free BSFL and non-sterile BSFL could achieve 31.71% and 88.72% AFB₁ degradation, respectively, which indicated the important role of larvae gut microbiota in AFB₁ degradation. Furthermore, twenty-five AFB₁-degrading bacteria were isolated from BSFL gut, and S. acidaminiphila A2 achieved the highest AFB₁ degradation, by 94%. When S. acidaminiphila A2 was re-inoculated to BSFL, the detrimental effect of AFB₁ on the growth performance of BSFL was alleviated, and complete AFB₁ degradation in peanut meal was obtained. In conclusion, the present study may provide a strategy to degrade AFB₁ in feedstuff through bioconversion with BSFL in combination with gut-originated AFB₁-degrading bacteria, while providing a sustainable insect protein and fat source to animals.

Background: Hexavalent chromium (Cr(VI)) can migrate into soil and water, posing risks to animal health. However, it remains unclear whether Cr(VI) perturbs essential trace elements and antioxidant gene expression, triggers apoptosis, or disrupts hepatic lipid metabolism in New Zealand rabbits. Methods: To address this knowledge gap, twenty-four 30-day-old New Zealand rabbits were randomly allocated to one control and three Cr(VI)-treated groups (differing in Cr(VI) concentration) and maintained for 28 days. Livers were then harvested for analysis. Total Cr and essential trace elements were quantified by ICP-OES. Hematoxylin–eosin staining and transmission electron microscopy were employed to assess histopathological and ultrastructural alterations, respectively. Hepatic lipid accumulation was visualized with Oil Red O staining. QRT-PCR was used to determine the expression of antioxidant and lipid-metabolism-related genes. Results: Cr(VI) was detectable in liver tissue at all exposure levels and was accompanied by significant decreases in four essential trace elements (Fe, Mn, Zn, and Se); Cu displayed a biphasic response, rising at lower Cr(VI) doses before declining at higher doses. Histopathological and ultrastructural analyses revealed overt hepatic injury. Notably, all Cr(VI) treatments elevated antioxidant gene expression, indicating activation of hepatic defense pathways. Lipid metabolism was also disrupted, evidenced by increased lipid deposition and up-regulation of genes governing hepatic fat metabolism. Conclusions: Collectively, these findings demonstrate that Cr(VI) elicits dose-dependent activation of hepatic antioxidant defenses, promotes apoptosis, and induces lipid-metabolic disorders in New Zealand rabbit hepatocytes. This study provides novel mechanistic insights into Cr(VI)-induced hepatotoxicity and offers a valuable reference for evaluating the hepatic risks of environmental Cr(VI) exposure in this species.

In this study, the RUSITEC system was used to study the regulation of rumen-derived Pseudomonas sp. PSC001 (PSC001) on the rumen environment contaminated by Zearalenone (ZEN). The rumen fluid of dairy cows was selected as the fermentation broth, and four experimental groups were set up: control group (CON), Pseudomonas group (PS), ZEN pollution group (ZEN), and PS and ZEN co-treatment group (PS + ZEN). The NH₃-N, microbial protein (MCP), and volatile fatty acid (VFA) in the rumen fermentation broth were measured after culturing, and the changes in microbial community structure in rumen fluid were analyzed by 16S rRNA gene sequencing. After adding PSC001, the concentration of propionic acid, valeric acid, and butyric acid increased, and the acetate to propionate ratio and concentration of isovaleric acid decreased. ZEN exposure can lead to an abnormal increase in NH₃-N, valeric acid, and isovaleric acid content and a decrease in MCP content. The content of NH₃-N, valeric acid, and isovaleric acid decreased and the content of MCP increased in the PS + ZEN combined treatment group. The addition of PSC001 and ZEN significantly or extremely significantly increased the abundance of 18 genera and significantly or extremely significantly decreased the relative abundance of 5 genera in rumen fluid, respectively. It is worth noting that with the addition of both at the same time, the abundance of four genera in the PS + ZEN group was significantly or extremely significantly increased among the five genera with decreased abundance in the ZEN group. Among the 18 genera with increased abundance in the ZEN group, 10 genera in the PS + ZEN group decreased significantly or extremely significantly. In summary, the addition of PSC001 alleviated the negative impact of ZEN on the internal environment of rumen fermentation, and it also had a positive regulatory effect on rumen fermentation.

Aflatoxin B₁ (AFB₁) causes acute liver injury in livestock. This study evaluated whether Vitamin U could alleviate AFB₁-induced hepatotoxicity in mice. AFB₁ (3 mg/kg) reduced PLT, PCT, and EOS counts, caused hepatic vascular congestion, and decreased GSH-Px activity. Vitamin U (50 mg/kg) significantly improved these hematological parameters, alleviated central venous and sinusoidal congestion, increased T-SOD activity and upregulated IL-10 mRNA expression. However, Vitamin U did not significantly reverse AFB₁-induced elevation of ALP or reduction in GSH-Px, nor did it affect ALT, AST, or protein levels of the Nrf2/Keap1 pathway. Transcriptomic analysis revealed enrichment of DEGs in immune- and cell cycle-related pathways, with no direct enrichment observed in the Nrf2/Keap1 pathway. Vitamin U upregulated Keap1 mRNA expression but did not alter KEAP1 protein levels. In conclusion, Vitamin U partially protects against AFB₁-induced acute liver injury by ameliorating thrombocytopenia, vascular congestion, enhancing T-SOD activity, and upregulating IL-10 expression, providing preliminary experimental evidence for further investigation.