Deoxynivalenol Exposure Leads to Abnormal Renal Tubular Autophagy Flow

Abstract Deoxynivalenol (DON) is one of the common mycotoxins contaminating feed. Renal tubular epithelial cells may experience oxidative stress as a result of consuming DON over time. However, little is known about the biological mechanisms through which DON results in kidney damage. This study employed proteomics, atomic force microscope (AFM), transmission electron microscope (TEM), and fluorescent probes, among other techniques, to reveal that DON exposure caused disturbances in renal autophagy flux both in vivo and in vitro. Mechanistically, this study found that DON exposure led to impaired formation of autophagosomes in the kidney. In addition, superoxide production by damaged mitochondria reduces ferroptosis resistance in renal tubules, and intracellular Fe ²⁺ accumulates toward lysosomes, leading to impaired lysosomal function. This results in further disruption of autophagy flux. In summary, these findings substantiate the pivotal role of autophagy in renal injury induced by DON exposure, preliminarily elucidate the underlying mechanisms by which DON exposure triggers renal damage, and offer therapeutic strategies for its prevention and treatment.