Vitamin E Attenuates Red-Light-Mediated Vasodilation: The Benefits of a Mild Oxidative Stress

Author:

Keszler Agnes1,Weihrauch Dorothee12ORCID,Lindemer Brian1ORCID,Broeckel Grant1ORCID,Lohr Nicole L.13456

Affiliation:

1. Department of Medicine, Division of Cardiovascular Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA

2. Department of Plastic Surgery, Medical College of Wisconsin, Milwaukee, WI 53226, USA

3. Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA

4. Clement J. Zablocki VA Medical Center, Milwaukee, WI 53295, USA

5. Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL 53233, USA

6. Birmigham VA Medical Center, Birmingham, AL 53233, USA

Abstract

Red light (670 nm) energy controls vasodilation via the formation of a transferable endothelium-derived nitric oxide (NO)-precursor-containing substance, its intracellular traffic, and exocytosis. Here we investigated the underlying mechanistic effect of oxidative stress on light-mediated vasodilation by using pressure myography on dissected murine arteries and immunofluorescence on endothelial cells. Treatment with antioxidants Trolox and catalase decreased vessel dilation. In the presence of catalase, a lower number of exosomes were detected in the vessel bath. Light exposure resulted in increased cellular free radical levels. Mitochondrial reactive oxygen species were also more abundant but did not alter cellular ATP production. Red light enhanced the co-localization of late exosome marker CD63 and cellular S-nitrosoprotein to a greater extent than high glucose, suggesting that a mild oxidative stress favors the localization of NO precursor in late exosomes. Exocytosis regulating protein Rab11 was more abundant after irradiation. Our findings conclude that red-light-induced gentle oxidative stress facilitates the dilation of blood vessels, most likely through empowering the traffic of vasodilatory substances. Application of antioxidants disfavors this mechanism.

Funder

NHLBI HL13955

Veteran Health Administration

Publisher

MDPI AG

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