A preliminary study on the pathology and molecular mechanism of fumonisin B1 nephrotoxicity in young quails.

Fumonisin B1 (FB1) is a widely present mycotoxin that accumulates in biological systems and poses a health risk to animals. However, few studies have reported the molecular mechanism by which FB1 induces nephrotoxicity. The aim of this study was to assess the extent of nephrotoxicity during FB1 exposure and the possible molecular mechanisms behind it. Therefore, 180 young quails were equally divided into two groups. The control group was fed typical quail food, while the experimental group was fed quail food containing 30 mg·kg-1 FB1. Various parameters were assessed, which included histopathological, ultrastructural changes, levels of biochemical parameters, oxidative indicators, inflammatory factors, possible target organelles mitochondrial and endoplasmic reticulum (ER)-related factors, nuclear xenobiotic receptors (NXR) response, and cytochrome P450 system (CYP450s)-related factors in the kidneys on days 14, 28, and 42. The results showed that FB1 can induce oxidative stress through NXR response and disorder of the CYP450s system, leading to mitochondrial dysfunction and ER stress, promoting the expression of inflammatory factors (including IL-1ß, IL-6, and IL-8) and causing kidney damage. This study elucidated the possible molecular mechanism by which FB1 induces nephrotoxicity in young quails.

Antagonistic Effect of Selenium on Fumonisin B1 Promotes Neutrophil Extracellular Traps Formation in Chicken Neutrophils.

Neutrophils are an important component of the innate immune system, and one of their defense mechanisms, neutrophil extracellular traps (NETs), is a hot topic of the current research. This study explored the effects of fumonisin B1 (FB1) on chicken neutrophil production of NETs and its possible molecular mechanism of action. Scanning electron microscopy and fluorescence microscopy were used to observe morphological changes in neutrophils, and a fluorescence microplate reader was used to detect reactive oxygen species (ROS) and extracellular DNA release from neutrophils. Quantitative PCR (qPCR) and western blot were used to determine the expression levels of selenoproteins. The results indicate that FB1 inhibited the zymosan-induced formation of NETs in chicken neutrophils by preventing ROS burst and histone H3 (H3) and neutrophil elastase (NE) release. Moreover, the mRNA expression levels of glutathione peroxidase (GPX), thioredoxin reductase (TXNRD), and deiodinase (DIO) were downregulated in the FB1 group. The protein expression levels of GPX1, GPX2, GPX3, DIO3, and TXNRD1 were consistent with the changes in their gene expressions, suggesting an abnormal selenoprotein expression in response to the toxic effects of FB1. Conversely, selenium (Se) supplementation reduced the toxic effects of FB1 and restored the NETs formation, indicating that Se can be used as a potential drug to prevent and control FB1 toxicity in livestock farming.

Fumonisin B1 induces hepatotoxicity in mice through the activation of oxidative stress, apoptosis and fibrosis.

Fumonisin B1 (FB1) is a harmful environmental pollutant that induces hepatotoxicity, but the mechanism is still poorly understood. Therefore, the aim of this work was to investigate the effects of FB1 on the liver of mice and discover the underlying molecular mechanisms. A total of 40 male mice were exposed to 0 or 5 mg/kg FB1 for 42 days, and then, they were sacrificed, and the liver and blood were collected. Besides, AML12 cells were exposed to FB1. Biochemical and liver related indexes as well morphological changes, redox, apoptosis and fibrosis related markers were measured in liver and AML12 cells. The results showed that the liver function and biochemical indexes in the blood were changes, and the histopathological analysis indicated that FB1 exposure caused hepatic sinusoid atrophy, hemosiderosis, hepatocyte steatosis and fibrosis, finally inducing liver injury. Notably, a significant increase in the intracellular antioxidant enzymes SOD1, SOD2, NF-κB (p65), H2O2 and NO was found in FB1 exposed AML12 cells and liver tissues. In addition, TUNEL staining showed many apoptotic cells, and western blotting revealed a significant increase in the pro-apoptosis proteins. FB1 also induced liver fibrosis by triggering TGF-ß1/α-SMA/collagen/MMP signaling in the hepatocytes. Our results provide a novel explanation of the toxicological mechanism of action of FB1, which provoked oxidative stress, apoptosis and fibrosis in mice liver.