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Isabella Panfoli, Daniela Calzia, Federico Caicci, Lucia Manni, Paolo Degan, Silvia Ravera, Martina Bartolucci, Paola Ramoino, Carlo Enrico Traverso; Inhibition of Rod Outer Segment ectopic FoF1-ATP synthase by polyphenolic phytochemicals: new Insights on Oxidative Stress-related Retinopathies.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):386.
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The effect of natural polyphenolic phytochemicals, known antioxidants, was studied on the ectopic ATPase/ATP synthase activity of the retinal rod Outer Segments (OS). The OS is a specialized organelle capable of phototransduction. Our previous studies on purified bovine OS disks reported an extramitochondrial oxidative phosphorylation (OXPHOS) therein . Notably, OXPHOS can become a major source of oxidative stress, a common cause of retinal pathologies.
The rod OS ATPase/ATP synthase activities were investigated by luminometry and oxymetry on OS homogenates. The expression of OXPHOS proteins in the OS was studied by electron transmission and fluorescence confocal microscopy on bovine retinal sections.
Resveratrol, a stilbene phytoalexin present in grapes and red wine, and curcumin, a component of turmeric, inhibited ATP synthase activity by 90% and 20%, respectively. Co-administration of piperine, a major alkaloid of black pepper, with curcumin enhanced ATP synthesis inhibition (up to 56%). Piperine alone displayed no effect. ATPase activity, tested in purified OS in the presence of ouabain, inhibitor of Na+/K+ATPase, was inhibited by epigallocatechin gallate, a catechin found in green tea, and quercetin, by 52% and 54% respectively.
The effect of polyphenols on the OS ATPase/ATP synthase activity suggests that these natural antioxidant substances significantly interact with the OS ATP synthase. Multiple lines of evidence indicate oxidative stress as a common source of retinal pathologies such as retinitis pigmentosa and age related macular degeneration, and glaucoma. Therefore, neuroprotective treatments with these polyphenols can be regarded under new light . references  I.. Panfoli et al. Int J Biochem Cell Biol. 2009; 41, 2555-65.  I. Panfoli . et al Med Hypotheses 2012, 78, 423-7
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