Search

Arsenic is a widely distributed ecotoxic pollutant that has been found to cause neurotoxicity in a variety of species. Gut-brain axis is a two-way information network between the gut microbiome and the brain, which is closely related to organismal health. However, the role of the gut-brain axis in arsenic-induced neurotoxicity remains largely unknown. In order to explore whether there is a relationship between brain and gut microbiota of meat ducks, we performed molecular biological detection including RT-qPCR and Western blot, as well as morphological detection including, HE staining and immunohistochemistry. Meanwhile, intestinal contents were analyzed using 16 S ribosomal RNA gene sequencing and analysis In this study, we investigated whether arsenic trioxide (ATO) can activate the gut microbiome-brain axis to induce intestinal and brain injury. The results showed that ATO-exposure disrupted the diversity balance of intestinal microbiota and integrity and injured the intestinal structure. ATO-exposure also reduced the number of glycogen and goblet cells in the duodenum. In addition, exposure to ATO caused intestinal inflammatory injury by activating NF-κB signaling pathway and promoting the expression of its target genes. Meanwhile, the tight junction-related proteins (ZO-1, occludin) of gut and brain were reduced by ATO exposure. Furthermore, results also revealed that ATO-exposure induced brain injury, including neuronal cell vacuolization and reduced numbers of neuronal cells in the cortex and hippocampus. Remarkably, ATO-exposure also disrupted neurotransmitter levels. Additionally, our further molecular mechanism study revealed that ATO-exposure increased the expression of autophagy and apoptosis related mRNA and proteins levels in the brain tissues. Altogether, these findings provide a new insight into that ATO-exposure induced intestinal injury and aggravated neurotoxicity via the gut-brain axis. [Display omitted] • ATO exposure disrupted the diversity of gut microbiota. • ATO exposure induced inflammatory reaction in duodenum of duck. • Autophagy and apoptosis were involved in ATO-induced neurotoxicity. • Mechanism of gut-brain axis provided a novel insight into the arsenic toxicity. [ABSTRACT FROM AUTHOR]

Ducklings is one of the most susceptible poultry to Aflatoxin B1 (AFB1) which widely existed in duckling products will also in turn affect human health. Curcumin (CUR) has significant effects on immune regulation and anti-oxidation. But whether CUR alleviates toxic effects on duckling spleen induced by AFB1 remains largely unknown. In this study we treated duckings with AFB1 and CUR for 21 days before harvesting serum and spleen tissue for analyses. The results showed that AFB1 damaged the spleen tissue of ducklings by activating the NF-κB signaling pathway. And the addition of CUR not only promoted the growth of ducklings, but also enhanced the immune function of the spleen and reduced the damage of AFB1 to the spleen tissue. At the same time, CUR activated the Nrf2 signaling pathway, upregulated the expression of related antioxidant enzymes, inhibited the NF-kB signaling pathway, and ultimately reducing the inflammation of the duckling spleen induced by AFB1. It has been suggested from these results that Nrf2 pathway might be a potential therapeutic target for CUR to treat AFB1-induced immunosuppression in ducklings. [Display omitted] • Aflatoxin B1 exposure can induce immunotoxicity in duck spleen. • Curcumin can relieve the damage of Aflatoxin B1 to the spleen of ducklings. • The Nuclear factor erythroid 2-related factor 2 signaling pathway plays a vital role in the detoxification of Aflatoxin B1. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1) is the most prevalent and toxic class of aflatoxins, which is considered a significant risk factor for food safety. Curcumin, a phytoconstituent with anti-inflammatory and antioxidant properties, has potential therapeutic value for intestinal inflammatory diseases. In this study, the duckling model susceptible to AFB1 was selected for toxicity testing, aiming to explore the effect of curcumin on AFB1 enterotoxicity and its possible mechanism of action. The results showed that curcumin promoted the growth and development of ducklings and mitigated the changes in morphology and permeability serological index (DAO and D-LA) after AFB1 exposure. Curcumin also mitigated AFB1-induced oxidative stress by activating the Nrf2 pathway, and ameliorated intestinal inflammation by inhibiting the NF-κB/IκB signaling pathway and boosting intestinal autophagy. In terms of gut flora and their metabolites, we found that curcumin supplementation significantly increased the intestinal flora's abundance index and diversity index compared to the AFB1 group, mitigating the decline in the abundance of Actinobacteria and the rise in that of harmful bacteria Clostridia. Furthermore, untargeted metabolomic analysis revealed that the protective effect of curcumin on the intestine was mainly through the regulation of AFB1-induced disorders of lipid metabolism, involving linoleic acid metabolism, α-linolenic acid metabolism, and glycerolipid metabolism. Overall, the enteroprotective effects of curcumin may be of significant value in the future for treating chronic AFB1 poisoning and also provide new therapeutic ideas for other mycotoxicosis. [Display omitted] • AFB1 exposure induces oxidative stress, inflammation, and intestinal microflora disorders in the jejunum of ducks. • Curcumin alleviates enterotoxicity induced by AFB1 on ducks • Curcumin activates Nrf2 pathway and autophagy, inhibits NF-κB/IκB pathway, and improves jejunal microflora and metabolic disorders. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1), as the most toxic secondary metabolite produced by Aspergillus flavus, is a serious threat to human and animal health. Curcumin, a polyphenol from the plant turmeric, has demonstrated unique anti-damage properties in several studies. But, its ability to alleviate AFB1-induced liver damage in ducks and the underlying mechanisms are not completely elucidated. In this study, we investigated the intervention of curcumin on AFB1-induced hepatotoxicity in ducks. Research data showed that the combination of curcumin and AFB1 alleviated oxidative stress, reduced malondialdehyde (MDA) accumulation and relieved hepatotoxicity after 28 days of treatment, compared with AFB1. Also, curcumin upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant enzymes (SOD, HO-1), which enhanced the antioxidant capacity of the liver. In addition, curcumin inhibited AFB1-induced lysosomal damage in the liver, with the character of reduced lysosomal membrane permeabilization, restored autophagic flux, and promoted lysosomal biogenesis, thereby enhancing the self-protective capacity of the liver. In conclusion, our results suggest that curcumin alleviates AFB1-induced duck hepatotoxicity by inhibiting oxidative stress and lysosomal damage. [ABSTRACT FROM AUTHOR]

The ecological risks caused by the coexistence of pollutants such as arsenic (As) and polystyrene-nanoplastics (PSNPs) in the environment have become a non-negligible problem. However, the effects of As and PSNPs co-exposure on mammals and the underlying toxicity mechanisms have remained unclear. Therefore, the present study established mouse models of As and/or PSNPS exposure to systematically analyze the underlying role of autophagy, apoptosis and pyroptosis in hepatotoxicity induced by co-exposure of As and PSNPs. Our findings demonstrated for the first time that mice co-exposure to As and PSNPs displayed significant pathological changes in the liver, while exposure to As or PSNPs alone did not produce significant toxic effects. More importantly, As and PSNPs co-exposure activated excessive autophagy through altered expression levels of PI3K, mTOR, Beclin-1, ATG5, LC3 and P62. Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc). Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions. Overall, our findings provide deeper insight into the roles of apoptosis, pyroptosis and excessive autophagy in the aggravation of liver injury, which could contribute to a better understanding of the interactions between As and PSNPS exposure and the molecular mechanisms of hepatotoxicity. [Display omitted] • Co-exposure of As and PSNPS can induce hepatotoxicity and pose an ecological risk. • Excessive autophagy, apoptosis and pyroptosis synergizes to cell death. • Co-exposure to As and PSNP may have synergistic or additivity toxic effects. [ABSTRACT FROM AUTHOR]