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-1β, IL-6, and IL-8) and causing kidney damage. This study elucidated the possible molecular mechanism by which FB₁ induces nephrotoxicity in young quails.