Selective Activation of Endoplasmic Reticulum Stress by Reactive-Oxygen-Species-Mediated Ochratoxin A-Induced Apoptosis in Tubular Epithelial Cells.
Chong-Sun KhoiYu-Wen LinJia-Huang ChenBiing-Hui LiuTzu-Yu LinKuan-Yu HungChih-Kang ChiangPublished in: International journal of molecular sciences (2021)
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.
Keyphrases
- induced apoptosis
- endoplasmic reticulum stress
- oxidative stress
- reactive oxygen species
- high glucose
- cell death
- signaling pathway
- diabetic rats
- endothelial cells
- cell cycle arrest
- drug induced
- dna damage
- public health
- healthcare
- mental health
- climate change
- social media
- risk assessment
- cell proliferation
- human health
- pi k akt