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...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 22; no. 20; p. 11237
Main Authors Khoi, Chong-Sun, Chen, Jia-Huang, Lin, Tzu-Yu, Chiang, Chih-Kang, Hung, Kuan-Yu
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 18.10.2021
MDPI
Subjects
Animals
Apoptosis
Biomarkers
Carcinogens - toxicity
Cell cycle
DNA damage
Food contamination & poisoning
Humans
Kidney diseases
Kidney Diseases - chemically induced
Kidney Diseases - pathology
Kinases
Nitric oxide
Ochratoxins - toxicity
Oxidative stress
Plasma
Proteins
Review
Urine
ochratoxin A
molecular interaction
nephrotoxicity
prevention
Online AccessGet full text

Cover

More Information
Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
Contributed equally to this work.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms222011237