Aya Yokomakura, Jangja Hong, Kazuo Ohuchi, Seong-Eun Oh, Jin-Yong Lee, Nariyasu Mano, Tsutomu Takahashi, Gi-Wook Hwang, Akira Naganuma
Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, Tohoku University, Aoba-ku, Sendai, Miyagi, Japan.
The Journal of toxicological sciences 2012Treatment of the mouse leukemic cell line RAW 264 with bafilomycin A1 or concanamycin A, inhibitors of vacuolar-type (H(+))-ATPases (V-ATPases), significantly increased the production of reactive oxygen species (ROS) and decreased cell viability. These effects were significantly suppressed by the presence of N-acetyl cysteine (NAC), an ROS scavenger. si-RNA mediated knockdown of the gene for the c subunit of the V0 domain of V-ATPase also resulted in an increase in ROS production and a decrease in cell viability. These results suggest that decreased cellular V-ATPase activity decreases cell viability by increasing ROS production in RAW 264 cells.
Aya Yokomakura, Jangja Hong, Kazuo Ohuchi, Seong-Eun Oh, Jin-Yong Lee, Nariyasu Mano, Tsutomu Takahashi, Gi-Wook Hwang, Akira Naganuma. Increased production of reactive oxygen species by the vacuolar-type (H(+))-ATPase inhibitors bafilomycin A1 and concanamycin A in RAW 264 cells. The Journal of toxicological sciences. 2012;37(5):1045-8
PMID: 23038011
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