THE ROLE OF OXYGEN AND OXYGEN RADICALS IN THE BIOSYNTHESIS AND REGULATION OF MITOCHONDRIAL AND CYTOPLASMIC SUPEROXIDE DISMUTASE IN EUKARYOTES

1998 ◽

Vol 84 (5) ◽

pp. 1589-1595 ◽

Cited By ~ 14

Author(s):

William G. Mayhan ◽

Glenda M. Sharpe

Keyword(s):

Nitric Oxide ◽

Superoxide Dismutase ◽

Smokeless Tobacco ◽

Oxygen Radicals ◽

Cheek Pouch ◽

Hamster Cheek Pouch ◽

Macromolecular Transport ◽

Before And After ◽

Oxide Synthase

Nicotine, a major component of cigarettes and smokeless tobacco, has toxic effects on endothelium and impairs reactivity of resistance arterioles in response to agonists that stimulate the synthesis and/or release of nitric oxide. However, the effect of nicotine on nitric oxide synthase-dependent increases in macromolecular transport is not known. Thus our first goal was to determine the effect of nicotine on histamine-induced increases in macromolecular efflux. We used intravital microscopy and FITC dextran (mol wt 70,000) (FITC-dextran-70K) to examine macromolecular extravasation from postcapillary venules in response to histamine before and after intravenous infusion of vehicle or nicotine. Extravasation of macromolecules was quantitated by counting venular leaky sites and calculating clearance (ml/s × 10−6) of FITC-dextran-70K. Histamine elicited reproducible increases in venular leaky sites and clearance in hamsters infused with vehicle. In contrast, nicotine infusion inhibited histamine-induced increases in macromolecular efflux. Histamine (1.0 and 5.0 μM) elicited 19 ± 2 and 34 ± 4 vs. 3 ± 1 and 11 ± 5 leaky sites per 0.11 cm2, before vs. after nicotine infusion, respectively ( P < 0.05). Histamine-induced clearance of FITC-dextran-70K was also impaired after infusion of nicotine. Our second goal was to examine whether alterations in histamine-induced increases in macromolecular efflux by nicotine may be related to the production of oxygen radicals. Application of superoxide dismutase (150 U/ml) to the hamster cheek pouch restored histamine-induced increases in venular leaky sites and clearance of FITC-dextran-70K during infusion of nicotine. Thus nicotine alters agonist-induced increases in microvascular permeability, via the formation of oxygen radicals, to presumably inactivate nitric oxide.

Download Full-text

Superoxide dismutase restores endothelium-dependent arteriolar dilatation during acute infusion of nicotine

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.4.1292 ◽

1998 ◽

Vol 85 (4) ◽

pp. 1292-1298 ◽

Cited By ~ 40

Author(s):

William G. Mayhan ◽

Glenda M. Sharpe

Keyword(s):

Superoxide Dismutase ◽

Free Radicals ◽

Topical Application ◽

Oxygen Radicals ◽

Cheek Pouch ◽

Oxygen Derived Free Radicals ◽

Before And After

We previously showed [ Am. J. Physiol. 272 ( Heart Circ. Physiol. 41): H2337–H2342, 1997] that nicotine impairs endothelium-dependent arteriolar dilatation. However, mechanisms that accounted for the effect of nicotine on endothelium-dependent vasodilatation were not examined. Thus the goal of this study was to examine the role of oxygen radicals in nicotine-induced impairment of arteriolar reactivity. We measured diameter of cheek pouch resistance arterioles (∼50 μm diameter) in response to endothelium-dependent (ACh and ADP) and -independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine in the absence or presence of superoxide dismutase. ACh, ADP, and nitroglycerin produced dose-related dilatation of cheek pouch arterioles before infusion of vehicle or nicotine. Infusion of vehicle, in the absence or presence of superoxide dismutase (150 U/ml), did not alter endothelium-dependent or -independent arteriolar dilatation. In contrast, infusion of nicotine (2 μg ⋅ kg−1 ⋅ min−1) impaired endothelium-dependent, but not -independent, arteriolar dilatation. In addition, the effect of nicotine on endothelium-dependent vasodilatation was reversed by topical application of superoxide dismutase. We suggest that nicotine impairs endothelium-dependent arteriolar dilatation via an increase in the synthesis/release of oxygen-derived free radicals.

Download Full-text

Oxygen Radicals Do Not Play a Role in Arteriolar Dilation during Cortical Spreading Depression

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199601000-00021 ◽

1996 ◽

Vol 16 (1) ◽

pp. 175-179 ◽

Cited By ~ 5

Author(s):

Wei Meng ◽

David W. Busija

Keyword(s):

Superoxide Dismutase ◽

Cortical Spreading Depression ◽

Oxygen Radicals ◽

Spreading Depression ◽

Oxygen Radical ◽

Onset Latency ◽

Radical Scavengers ◽

Cranial Window ◽

Cerebral Arterioles

This study examined the role of oxygen radicals in pial arteriolar changes during cortical spreading depression (CSD). CSD was induced by microinjection of 5% KCl in anesthetized adult rabbits. Pial diameter was measured with a closed cranial window and intravital microscopy. During control CSD (n = 12), the dilation amplitude and area were 55 ± 14% and 693 ± 69 mm2 (baseline = 76 ± 14 μm), respectively. Oxygen radical scavengers, superoxide dismutase (SOD; 105 U/ml, topical application; n = 5) or oxypurinol (50 mg/kg i.v.; n = 7), did not alter the dilation amplitude and area or change onset latency during CSD. Further, SOD and oxypurinol did not prevent NG-nitro-L-arginine from attenuating arteriolar dilation during CSD (n = 12). We conclude that oxygen radicals do not play a role in the transient dilation of cerebral arterioles during CSD.

Download Full-text

Role of Superoxide Dismutase in Otitis Media with Effusion

Annals of Otology Rhinology & Laryngology ◽

10.1177/000348949810700411 ◽

1998 ◽

Vol 107 (4) ◽

pp. 327-331 ◽

Cited By ~ 20

Author(s):

Hideo Shigemi ◽

Toru Egashira ◽

Yuichi Kurono ◽

Goro Mogi

Keyword(s):

Superoxide Dismutase ◽

Otitis Media ◽

Oxygen Radicals ◽

Otitis Media With Effusion ◽

Middle Ear Effusion ◽

Significant Difference ◽

Spin Resonance ◽

Trapping Method ◽

Ear Effusion

The concentration of superoxide dismutase (SOD) in middle ear effusion (MEE) was measured by the electron spin resonance trapping method in order to clarify the role of SOD in otitis media with effusion (OME) in children. The SOD levels in mucoid MEEs were significantly higher than those in serous and purulent MEEs. There was no significant difference in the levels of SOD between neutrophil-dominant MEEs and mononuclear cell-dominant MEEs, and the levels were negatively correlated with the number of neutrophils in the MEEs. Moreover, the levels were significantly increased in patients having recurrence of MEE within 3 months compared with patients without recurrence of MEE. Although it is known that SOD plays an important role in protecting the host from oxygen radicals, the findings in this study suggest that SOD might be related to the chronicity of OME.

Download Full-text