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Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence

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 intracellu...

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Autores principales: Khoi, Chong-Sun, Chen, Jia-Huang, Lin, Tzu-Yu, Chiang, Chih-Kang, Hung, Kuan-Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8539333/
https://www.ncbi.nlm.nih.gov/pubmed/34681895
http://dx.doi.org/10.3390/ijms222011237
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author Khoi, Chong-Sun
Chen, Jia-Huang
Lin, Tzu-Yu
Chiang, Chih-Kang
Hung, Kuan-Yu
author_facet Khoi, Chong-Sun
Chen, Jia-Huang
Lin, Tzu-Yu
Chiang, Chih-Kang
Hung, Kuan-Yu
author_sort Khoi, Chong-Sun
collection PubMed
description 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.
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spelling pubmed-85393332021-10-24 Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence Khoi, Chong-Sun Chen, Jia-Huang Lin, Tzu-Yu Chiang, Chih-Kang Hung, Kuan-Yu Int J Mol Sci Review 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. MDPI 2021-10-18 /pmc/articles/PMC8539333/ /pubmed/34681895 http://dx.doi.org/10.3390/ijms222011237 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Khoi, Chong-Sun
Chen, Jia-Huang
Lin, Tzu-Yu
Chiang, Chih-Kang
Hung, Kuan-Yu
Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title_full Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title_fullStr Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title_full_unstemmed Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title_short Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence
title_sort ochratoxin a-induced nephrotoxicity: up-to-date evidence
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8539333/
https://www.ncbi.nlm.nih.gov/pubmed/34681895
http://dx.doi.org/10.3390/ijms222011237
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