The science team at MitoQ, and independent scientists, have thoroughly evaluated this study and can confidently advise that the results of this paper were the result of experimental MitoQ administration in a very specific test tube environment, and need not be a concern for those taking MitoQ as a dietary supplement.
This study was conducted in isolated cells (individual animal cells removed from tissue and cultured) and not within a functioning kidney inside a body, and the MitoQ was administered at concentrations many times higher than would ever be taken as a supplement.
The recommended daily dose of MitoQ is 10-20 mg per day and MitoQ has been studied at 80 mg per day for up to a year in elderly patients with an excellent safety profile. The kidney study in question administered MitoQ at a level of 500 nmol/L, which is significantly higher than would ever reach cells in your body when taken at the recommended daily dose.
If you incubated cells in a solution containing sugar at levels much higher than normal consumption would expose them to, this would similarly have a negative effect on the cells, but that’s not relevant to the normal daily consumption of sugar.
For almost two decades MitoQ has been extensively evaluated for safety and has been shown to be protective of the kidneys in several studies and also during organ storage. MitoQ is also currently being evaluated in two human trials to assist with kidney health at The University of Delaware and Virginia Commonwealth University. These patients have chronic kidney disease so would be even more vulnerable than those with normal kidney function and these trials would not have been approved if the consensus was that MitoQ was unsafe.
You can read more about these trials here:
Please also find below a list of published peer-reviewed studies which show that MitoQ supports normal kidney function. If you should have any further concerns, please contact our customer support team here: https://www.mitoq.com/contact.
Wnt/β-catenin/RAS signalling mediates age-related renal fibrosis and is associated with mitochondrial dysfunction. Miao J et al. Aging Cell. 2019;00:e13004. DOI: 10.111/acel.13004
Mitochondria-targeted antioxidant MitoQ reduced renal damage caused by ischemia-reperfusion injury in rodent kidneys: Longitudinal observations of T2 -weighted imaging and dynamic contrast-enhanced MRI. Liu X et al. Magn Reson Med. 2018 Mar; 79(3):1559-1567. DOI: 10.1002/mrm.26772
Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ROS-TXNIP-NLRP3 biological axis. Han Y et al. Redox Biol. 2018 Feb 15;16: 32-46. DOI: 10.1016/j.redox.2018.02.013
Mitochondrial abnormality facilitates cyst formation in autosomal dominant polycystic kidney disease. Ishimoto Y et al. Mol. Cell. Biol. 2017 Dec. 37: 24 e00337-17. DOI: 10.1128/MCB.00337-1
Evaluation of a novel mitochondria-targeted anti-oxidant therapy for ischaemia-reperfusion injury in renal transplantation. Hamed, M. O. Doctoral thesis. Sep 2017. DOI: 10.17863/CAM.13853
The mitochondria-targeted antioxidant MitoQ ameliorated tubular injury mediated by mitophagy in diabetic kidney disease via Nrf2/PINK1. Xiao L et al. Redox Biol. 2017 Apr; 11: 297–311. DOI: 10.1016/j.redox.2016.12.022
Targeted mitochondrial therapy using MitoQ shows equivalent renoprotection to angiotensin converting enzyme inhibition but no combined synergy in diabetes. Ward MS et al. Scientific Reports 2017. 7: 15190. DOI: 10.1038/s41598-017-15589-x
The swan-neck lesion: proximal tubular adaptation to oxidative stress in nephropathic cystinosis. Galaretta CI et al. Am J Physiol Renal Physiol. 2015 May 15;308(10): F1155-66. DOI: 10.1152/ajprenal.00591.2014
Protection against renal ischemia–reperfusion injury in vivo by the mitochondria targeted antioxidant MitoQ. Dare AJ et al. Redox Biol. 2015 Aug; 5: 163–168. DOI: 10.1016/j.redox.2015.04.008
Contribution of mitochondrial function to exercise-induced attenuation of renal dysfunction in spontaneously hypertensive rats. Gu Q et al. Mol Cell Biochem. 2015 Aug; 406(1-2):217-25. DOI: 10.1007/s11010-015-2439-6
Peroxynitrite induced mitochondrial biogenesis following MnSOD knockdown in normal rat kidney (NRK) cells. Marine A et al. Redox Biol. 2014; 2: 348–357. DOI: 10.1016/j.redox.2014.01.014
Mitochondrial targeted antioxidant MitoQ modulates Smad2/3 and β-catenin signaling pathways in the prevention of diabetes induced kidney damage. Reily C. Free Radic Biol Med. 2014; 49:S40. DOI: 10.1016/j.freeradbiomed.2010.10.083
Preclinical evaluation of the mitochondria-targeted antioxidant mitoquinone to treat sepsis-induced acute kidney injury. Patil NK et al. FASEB J. 2013 27:1_supplement, 889.8-889.8
MitoQ Blunts Mitochondrial and Renal Damage during Cold Preservation of Porcine Kidney. Parajuli N et al. PLoS ONE. 2012;7(11). DOI:10.1371/journal.pone.0048590
The Mitochondria-targeted Antioxidant Mitoquinone Protects Against Cold Storage Injury of Renal Tubular Cells and Rat Kidney. Mitchell T et al. J Pharmacol Exp Ther. 2011;336(3):682-692. DOI: 10.1124/jpet.110.176743
Prevention of diabetic nephropathy in Ins2+/−AkitaJ mice by the mitochondria-targeted therapy MitoQ. Chacko BK et al. Biochem J. 2010 Nov 15; 432(Pt 1): 9–19. DOI: 10.1042/BJ20100308
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