title: Antioxidant Properties of Whole Body Periodic Acceleration (pGz).
abstract: The recognition that oxidative stress is a major component of several chronic diseases has engendered numerous trials of antioxidant therapies with minimal or no direct benefits. Nanomolar quantities of nitric oxide released into the circulation by pharmacologic stimulation of eNOS have antioxidant properties but physiologic stimulation as through increased pulsatile shear stress of the endothelium has not been assessed. The present study utilized a non-invasive technology, periodic acceleration (pGz) that increases pulsatile shear stress such that upregulation of cardiac eNOS occurs, We assessed its efficacy in normal mice and mouse models with high levels of oxidative stress, e.g. Diabetes type 1 and mdx (Duchene Muscular Dystrophy). pGz increased protein expression and upregulated eNOS in hearts. Application of pGz was associated with significantly increased expression of endogenous antioxidants (Glutathioneperoxidase-1(GPX-1), Catalase (CAT), Superoxide, Superoxide Dismutase 1(SOD1). This led to an increase of total cardiac antioxidant capacity along with an increase in the antioxidant response element transcription factor Nrf2 translocation to the nucleus. pGz decreased reactive oxygen species in both mice models of oxidative stress. Thus, pGz is a novel non-pharmacologic method to harness endogenous antioxidant capacity.
authors.affiliation: Division of Neonatology, Mount Sinai Medical Center, Miami Beach, Florida, United States of America.
authors.forename: Arkady
authors.initials: A
authors.lastname: Uryash
authors.affiliation: Division of Neonatology, Mount Sinai Medical Center, Miami Beach, Florida, United States of America.
authors.forename: Jorge
authors.initials: J
authors.lastname: Bassuk
authors.affiliation: Department of Surgery, Columbia University, New York, New York, United States of America.
authors.forename: Paul
authors.initials: P
authors.lastname: Kurlansky
authors.affiliation: Department of Molecular Biosciences, University of California Davis, Davis, California, United States of America.
authors.forename: Francisco
authors.initials: F
authors.lastname: Altamirano
authors.affiliation: Department of Molecular Biosciences, University of California Davis, Davis, California, United States of America.
authors.forename: Jose R
authors.initials: JR
authors.lastname: Lopez
authors.affiliation: Division of Neonatology, Mount Sinai Medical Center, Miami Beach, Florida, United States of America.
authors.forename: Jose A
authors.initials: JA
authors.lastname: Adams
mesh_terms: D000054:Acceleration; D000818:Animals; D000975:Antioxidants / Q000032:analysis / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D015153:Blotting, Western; D002374:Catalase / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005979:Glutathione Peroxidase / Q000032:analysis; D006339:Heart Rate / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D020388:Muscular Dystrophy, Duchenne / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000737:chemistry; D051267:NF-E2-Related Factor 2 / Q000032:analysis; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000032:analysis; D013482:Superoxide Dismutase / Q000032:analysis; D000072105:Superoxide Dismutase-1; D000094765:Glutathione Peroxidase GPX1
chemical_list: D000975:Antioxidants; D051267:NF-E2-Related Factor 2; C495636:Nfe2l2 protein, mouse; D017382:Reactive Oxygen Species; D002374:Catalase; D005979:Glutathione Peroxidase; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D000094765:Glutathione Peroxidase GPX1; C000722068:Gpx1 protein, mouse