| Literature DB >> 31431058 |
Ji Hyun Yu1, Sun Woo Lim2,3, Kang Luo2,3, Sheng Cui2,3, Yi Quan2,3, Yoo Jin Shin2,3, Kyung Eun Lee4, Hong Lim Kim5, Eun Jeong Ko1,2,3, Byung Ha Chung1,2,3, Ju Hwan Kim6, Sang J Chung7, Chul Woo Yang1,2,3.
Abstract
The major side effect of tacrolimus (Tac) is nephrotoxicity. We studied whether supplementation of coenzyme Q10, (CoQ10) a potent antioxidant, can reduce Tac-induced nephrotoxicity via improving mitochondrial function. In an in vitro study, CoQ10 reduced the production of Tac-induced mitochondrial reactive oxygen species and abolished the loss of mitochondrial membrane potential in proximal tubular cell line. Assessment of mitochondrial function revealed that CoQ10 decreased oxygen consumption and mitochondrial respiration rate increased by Tac, suggesting improvement of mitochondrial function to synthesize ATP with CoQ10 treatment. The effect of the CoQ10 in vitro study was observed in an experimental model of chronic Tac-induced nephropathy. CoQ10 attenuated Tac-induced oxidative stress and was accompanied by function and histologic improvement. On electron microscopy, addition of CoQ10 increased not only the number but also the volume of mitochondria compared with Tac treatment only. Our data indicate that CoQ10 improves Tac-induced mitochondrial dysfunction in kidney. Supplementary CoQ10 treatment may be a promising approach to reduce Tac-induced nephrotoxicity.-Yu, J. H., Lim, S. W., Luo, K., Cui, S., Quan, Y., Shin, Y. J., Lee, K. E., Kim, H. L., Ko, E. J., Chung, B. H., Kim, J. H., Chung, S. J., Yang, C. W. Coenzyme Q10 alleviates tacrolimus-induced mitochondrial dysfunction in kidney.Entities:
Keywords: 3D reconstruction; nephrotoxicity; reactive oxygen species
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Year: 2019 PMID: 31431058 PMCID: PMC6902707 DOI: 10.1096/fj.201900386RR
Source DB: PubMed Journal: FASEB J ISSN: 0892-6638 Impact factor: 5.191