Description
SKQ1 (bromide) is a mitochondria-targeted antioxidant that decreases transmembrane potential and production of reactive oxygen species (ROS). SKQ1 prevents neuronal loss and synaptic damage in a rat model of spontaneous Alzheimer’s disease, as well as decreases severity of arthritic lesions in rats. SKQ1 slows development of age-related ocular pathologies in murine, porcine, bovine, and canine model systems. It also prevents acute phenoptosis following rhabdomyolysis, stroke, and myocardial infarction.
in vivo
Regarding systemic angiogenic factors, it is observed in serum of Pancreatic ductal adenocarcinoma (PDAC) bearing mice a decrease in KC in the group of continuous treatment with Visomitin (SkQ1). Treatment of the mice with Visomitin increases the level of VEGF molecules. The amount of MIP1a and prolactin is reduced in all Visomitin treatment groups or after the follow-up treatment, respectively. Also, an increase in the IL-6 and IL-13 amount is found in the Visomitin treated groups. TGF-b amount is decreased in the pretreatment setting. On the contrary, all schemes of the Visomitin treatment decrease the NKT cell percentage. The Visomitin treatment has prolonged the median survival of PDAC-bearing mice, but the difference does not reach the level of significance defined[1].
References
[1] SKULACHEV V P. Cationic antioxidants as a powerful tool against mitochondrial oxidative stress[J]. Biochemical and biophysical research communications, 2013, 441 2: Pages 275-279. DOI:
10.1016/j.bbrc.2013.10.063[2] N. STEFANOVA. An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology[J]. Aging (Albany NY), 2016, 41 1: 2713-2731. DOI:
10.18632/aging.101054[3] ALEXANDER A ANDREEV-ANDRIEVSKIY. Efficacy of Mitochondrial Antioxidant Plastoquinonyl-decyl-triphenylphosphonium Bromide (SkQ1) in the Rat Model of Autoimmune Arthritis.[J]. Oxidative Medicine and Cellular Longevity, 2016: 8703645. DOI:
10.1155/2016/8703645[4] M. V. SKULACHEV V. P S F F Severin. Receptor regulation of senile phenoptosis[J]. Biochemistry (Moscow), 2014, 79 10: 994-1003. DOI:
10.1134/s0006297914100022[5] E.Y. PLOTNIKOV. Mechanisms of nephroprotective effect of mitochondria-targeted antioxidants under rhabdomyolysis and ischemia/reperfusion[J]. Biochimica et biophysica acta. Molecular basis of disease, 2011, 1812 1: Pages 77-86. DOI:
10.1016/j.bbadis.2010.09.008[6] EGOR Y PLOTNIKOV. Protective effect of mitochondria-targeted antioxidants in an acute bacterial infection.[J]. Proceedings of the National Academy of Sciences of the United States of America, 2013, 110 33: E3100-8. DOI:
10.1073/pnas.1307096110[7] VLADIMIR P. SKULACHEV . An attempt to prevent senescence: A mitochondrial approach[J]. Biochimica et Biophysica Acta-Bioenergetics, 2009, 1787 5: Pages 437-461. DOI:
10.1016/j.bbabio.2008.12.008
