scholarly journals Hexavalent chromium targets mitochondrial respiratory chain complex I to induce reactive oxygen species-dependent caspase-3 activation in L-02 hepatocytes

2012 ◽  
Vol 30 (3) ◽  
pp. 629-635 ◽  
Author(s):  
FANG XIAO ◽  
YANHONG LI ◽  
LU DAI ◽  
YUANYUAN DENG ◽  
YUE ZOU ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hexavalent Chromium ◽  
Respiratory Chain ◽  
Complex I ◽  
Caspase 3 ◽  
Chain Complex ◽  
Mitochondrial Respiratory Chain ◽  
Oxygen Species ◽  
Respiratory Chain Complex ◽  
Mitochondrial Respiratory Chain Complex

scholarly journals Increased Mitochondrial Fragmentation Mediated by Dynamin-Related Protein 1 Contributes to Hexavalent Chromium-Induced Mitochondrial Respiratory Chain Complex I-Dependent Cytotoxicity

Toxics ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 50
Author(s):  
Yu Ma ◽  
Yujing Zhang ◽  
Yuanyuan Xiao ◽  
Fang Xiao
Keyword(s):  
Hexavalent Chromium ◽  
Respiratory Chain ◽  
Complex I ◽  
Chain Complex ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complex ◽  
Related Protein ◽  
Mitochondrial Fragmentation ◽  
Mitochondrial Respiratory Chain Complex ◽  
Mitochondrial Respiratory

Hexavalent chromium (Cr(VI)) pollution is a severe public health problem in the world. Although it is believed that mitochondrial fragmentation is a common phenomenon in apoptosis, whether excessive fission is crucial for apoptosis remains controversial. We previously confirmed that Cr(VI) mainly targeted mitochondrial respiratory chain complex I (MRCC I) to induce reactive oxygen species (ROS)-mediated apoptosis, but the related mechanism was unclear. In this study, we found Cr(VI) targeted MRCC I to induce ROS accumulation and triggered mitochondria-related cytotoxicity. Cr(VI)-induced cytotoxicity was alleviated by pretreatment of Glutamate/malate (Glu/Mal; MRCC I substrates), and was aggravated by cotreatment of rotenone (ROT; MRCC I inhibitor). Cr(VI) induced excessive mitochondrial fragmentation and mitochondrial dynamin-related protein 1 (Drp1) translocation, the application of Drp1-siRNA alleviated Cr(VI)-induced apoptosis. The cytotoxicity in the Drp1-si plus Cr(VI) treatment group was alleviated by the application of Glu/Mal, and was aggravated by the application of ROT. Drp1 siRNA promoted the inhibition of Glu/Mal on Cr(VI)-induced cytotoxicity, and alleviated the aggravation of ROT on Cr(VI)-induced cytotoxicity. Taken together, Cr(VI)-induced Drp1 modulation was dependent on MRCC I inhibition-mediated ROS production, and Drp1-mediated mitochondrial fragmentation contributed to Cr(VI)-induced MRCC I-dependent cytotoxicity, which provided the experimental basis for further elucidating Cr(VI)-induced cytotoxicity.

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