Abstract
Ochratoxin A (OTA) is a mycotoxin widely found in various foods and feeds that have a deleterious effect on humans and animals. It has been shown that OTA causes multiorgan toxicity, and the kidney is the main target of OTA among them. This present article aims to review recent and latest intracellular molecular interactions and signaling pathways of OTA-induced nephrotoxicity. Pyroptosis, lipotoxicity, organic anionic membrane transporter, autophagy, the ubiquitin-proteasome system, and histone acetyltransferase have been involved in the renal toxicity caused by OTA. Meanwhile, the literature reviewed the alternative or method against OTA toxicity by reducing ROS production, oxidative stress, activating the Nrf2 pathway, through using nanoparticles, a natural flavonoid, and metal supplement. The present review discloses the molecular mechanism of OTA-induced nephrotoxicity, providing opinions and strategies against OTA toxicity.
Highlights
Ochratoxin A (OTA) is a mycotoxin frequently found in various foods and animal feed [1,2,3,4]
This study showed in German infants, the mean OTA-aglycone concentration was 80 ± 14 ng/L, and OTA-total was 98 ± 114 ng/L after hydrolysis in German infants; in Turkish infants, the mean OTA-aglycone concentration was 285 ± 57 ng/L, and the mean value for OTA-total was 1041 ± 275 ng/L, same as a result in a German adult, urinary OTA levels were 76 ± 29; the OTA-total was 205 ± 114 ng/L, which implied that Ochratoxin A-8-β-glucuronide could be another biomarker to avoid underestimate
JAK2/STAT3 signaling pathway to induce apoptosis and DNA damage in PK15 cells and porcine alveolar macrophage (PAM); OTA increased the expression of suppressors of cytokine signaling 3 (SOCS3), which was regulated by DNA methyltransferase 1 (DNMT1) only in PK15 cells
Summary
Ochratoxin A (OTA) is a mycotoxin frequently found in various foods and animal feed [1,2,3,4]. Subsequent research showed no statistically significant evidence for the connection between OTA exposure and human health risks in the Bulgarian or Croatian study populations [11]. The animal study showed that chronic kidney disease (CKD) dogs had higher plasma OTA concentrations than healthy dogs. Ostry et al demonstrated that OTA was detected in human renal tissue with a level range from. The occurrence of OTA in a study in Poland demonstrated that low and constant OTA levels present in animal tissue and feed, implying continued exposure of OTA to animal and human beings [25]
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