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.

Background: Hexavalent chromium (Cr(VI)) is a widespread environmental toxic heavy metal with strong oxidative properties; however, its immunotoxicity and metabolic mechanisms in rabbit spleen remain largely unclear. Methods: In this study, New Zealand rabbits were exposed to 0, 12.5, 25, and 50 mg/L Cr(VI) (as potassium dichromate, K₂Cr₂O₇) via drinking water for four weeks to investigate splenic damage and the underlying molecular pathways. Spleen pathological injury was evaluated by hematoxylin and eosin (H&E) staining, and the distribution of T cells, B cells, and macrophages was assessed by immunohistochemistry. Antioxidant enzyme activities and antioxidant substance levels were determined using ELISA, and the relative mRNA expression of immune factor genes, antioxidant-related genes, and ferroptosis-related genes was quantified by quantitative real-time PCR (qRT-PCR). In addition, the distribution of iron in splenic tissue was detected by enhanced Prussian blue staining. Results: Our results demonstrate that high-dose Cr(VI) significantly inhibited body weight gain, induced lymphocyte atrophy, vacuolization, and widening of intercellular spaces in the splenic white pulp. Furthermore, Cr(VI) reduced T and B lymphocyte populations, promoted macrophage infiltration and inflammatory cytokine gene expression in a concentration-dependent manner, impaired total antioxidant capacity, and led to a decrease in glutathione (GSH) levels in the spleen. Additionally, Cr(VI) exposure increased iron accumulation, activated the ACSL4–NOX lipid peroxidation cascade, and downregulated GPX4 expression, ultimately triggering ferroptosis. Conclusions: These findings reveal that Cr(VI) causes splenic immune injury by disrupting oxidative homeostasis and inducing ferroptosis, providing novel insights for evaluating immunotoxicity and identifying metabolic targets under Cr(VI) pollution.

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.