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Takayuki Kamiya, Taiji Nagaoka, Tsuneaki Omae, Shinji Ono, Shinichi Otani, Akitoshi Yoshida; Benzo(e)Pyrene, a Toxic Element in Cigarette Smoke, Inhibits Endothelium-Dependent Nitric Oxide-Mediated Dilation of Porcine Retinal Arterioles Via Enhanced Superoxide Production. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4349.
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Recent epidemiologic studies have confirmed that cigarette smoking is a risk factor for ocular diseases, such as diabetic retinopathy and age-related macular degeneration. Moreover, the previous study has reported that benzo(e)pyrene (B(e)P), a toxic element in cigarette smoke, may cause cell death and induce apoptosis in retinal pigment epithelial cells in vitro. However, the direct effect of B(e)P on retinal microvasculature reactivity remains unknown. We investigated whether B(e)P affects endothelium-dependent nitric oxide (NO)-mediated dilation of retinal arterioles and if oxidative stress is involved in the B(e)P-mediated effect.
The porcine retinal arterioles were isolated, cannulated, and pressurized without flow for in vitro study. Diameter changes were recorded using videomicroscopic techniques.
Intraluminal treatment with B(e)P (1 mM, 180 minutes) significantly attenuated arteriolar dilation in response to the endothelium-dependent NO-mediated agonist bradykinin but not in response to endothelium-independent NO donor sodium nitroprusside. In the presence of the superoxide scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl, the detrimental effect of B(e)P on bradykinin-induced dilation was prevented.
B(e)P inhibits endothelium-dependent NO-mediated dilation in the retinal arterioles by producing superoxide. By impairing endothelium-dependent NO-mediated vasoreactivity, B(e)P potentially facilitates development of retinal vascular diseases.
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