期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 20, 页码 -出版社
MDPI
DOI: 10.3390/ijms222010951
关键词
ochratoxin A; ER stress; apoptosis; reactive oxygen species; HK-2 cell
资金
- National Taiwan University Hospital [NTUH-108-S4373, NTUH-UN-109-S4785, NTUH-110-S5074]
- NTUH-FEMH Joint research program [108-FTN16]
This study demonstrates that OTA induces nephrotoxicity through ER stress-related apoptosis in human renal cells, with a pathway mediated by ROS.
Ochratoxin A (OTA), one of the major food-borne mycotoxins, impacts the health of humans and livestock by contaminating food and feed. However, the underlying mechanism of OTA nephrotoxicity remains unknown. This study demonstrated that OTA induced apoptosis through selective endoplasmic reticulum (ER) stress activation in human renal proximal tubular cells (HK-2). OTA increased ER-stress-related JNK and precursor caspase-4 cleavage apoptotic pathways. Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Our results demonstrate that OTA induced ER stress-related apoptosis through an ROS-mediated pathway. This study provides new evidence to clarify the mechanism of OTA-induced nephrotoxicity.
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