Ochratoxin A (OTA) is a natural contaminant that has displayed nephrotoxicity and hepatotoxicity in mammals. It contaminates a great variety of foodstuffs and threatens people’s lives. The molecular mechanism of OTA-induced toxicity has been studied since 1965. Moreover, epigenetic mechanisms are also studied in OTA-induced toxicity. Additionally, the mode of OTA epigenetic research has been advanced in research hotspots. However, there is still no epigenetic study of OTA-induced toxicity. In this review, we discuss the relationship between these epigenetic mechanisms and OTA-induced toxicity. We found that studies on the epigenetic mechanisms of OTA-induced toxicity all chose the whole kidney or liver as the model, which cannot reveal the real change in DNA methylation or miRNAs or histone in the target sites of OTA. Our recommendations are as follows: (1) the specific target site of OTA should be detected by advanced technologies; and (2) competing endogenous RNAs (ceRNA) should be explored with OTA.

Ochratoxin A (OTA) displays nephrotoxicity and hepatotoxicity. However, in the acute toxicity rat model, there is no evidence on the relationship between OTA and nephrotoxicity and hepatotoxicity. Based on this, the integrated analysis of physiological status, damage biomarkers, oxidative stress, and DNA damage were performed. After OTA treatment, the body weight decreased and AST, ALP, TP, and BUN levels in serum increased. Hydropic degeneration, swelling, vacuolization, and partial drop occurred in proximal tubule epithelial cells. PCNA and Kim-1 were dose-dependently increased in the kidney, but Cox-2 expression and proliferation were not found in the liver. In OTA-treated kidneys, the mRNA expressions of Kim-1, Cox-2, Lcn2, and Clu were dose-dependently increased. The mRNA expressions of Vim and Cox-2 were decreased in OTA-treated livers. Some oxidative stress indicators were altered in the kidneys (ROS and SOD) and livers (SOD and GSH). DNA damage and oxidative DNA damage were not found. In conclusion, there is a limited link between oxidative stress and OTA-induced renal injury in an acute toxicity rat model.

Hexafluoropropylene Oxide Dimer Acid (HFPO-DA or GenX) is a pervasive perfluorinated compound with scant understood toxic effects. Toxicological studies on GenX have been conducted using animal models. To research deeper into the potential toxicity of GenX in humans and animals, we undertook a comprehensive analysis of transcriptome datasets across different species. A rank-in approach was utilized to merge different transcriptome datasets, and machine learning algorithms were employed to identify key genetic mechanisms common among various species and humans. We identified seven genes—TTR, ATP6V1B1, EPHX1, ITIH3, ATXN10, UBXN1, and HPX—as potential variables for classification of GenX-exposed samples, and the seven genes were verified in separate datasets of human, mouse, and rat samples. Bioinformatic analysis of the gene dataset further revealed that mitochondrial function and metabolic processes may be modulated by GenX through these key genes. Our findings provide insights into the underlying genetic mechanisms and toxicological impacts of GenX exposure across different species and offer valuable references for future studies using animal models to examine human exposure to GenX.