Antioxidant protection of NO‐induced relaxations of the mouse anococcygeus against inhibition by superoxide anions, hydroquinone and carboxy‐PTIO
E Lilley, A Gibson - British journal of pharmacology, 1996 - Wiley Online Library
E Lilley, A Gibson
British journal of pharmacology, 1996•Wiley Online Library1 The potential protective effect of several antioxidants [Cu/Zn superoxide dismutase (Cu/Zn
SOD), ascorbate, reduced glutathione (GSH), and α‐tocopherol (α‐TOC)] on relaxations of
the mouse anococcygeus muscle to nitric oxide (NO; 15 μm) and, where appropriate,
nitrergic field stimulation (10 Hz; 10 s trains) was investigated. 2 The superoxide anion
generating drug duroquinone (100 μm) reduced relaxations to exogenous NO by 54±6%;
this inhibition was partially reversed by Cu/Zn SOD (250 u ml− 1), and by ascorbate (500 …
SOD), ascorbate, reduced glutathione (GSH), and α‐tocopherol (α‐TOC)] on relaxations of
the mouse anococcygeus muscle to nitric oxide (NO; 15 μm) and, where appropriate,
nitrergic field stimulation (10 Hz; 10 s trains) was investigated. 2 The superoxide anion
generating drug duroquinone (100 μm) reduced relaxations to exogenous NO by 54±6%;
this inhibition was partially reversed by Cu/Zn SOD (250 u ml− 1), and by ascorbate (500 …
- 1The potential protective effect of several antioxidants [Cu/Zn superoxide dismutase (Cu/Zn SOD), ascorbate, reduced glutathione (GSH), and α‐tocopherol (α‐TOC)] on relaxations of the mouse anococcygeus muscle to nitric oxide (NO; 15 μm) and, where appropriate, nitrergic field stimulation (10 Hz; 10 s trains) was investigated.
- 2The superoxide anion generating drug duroquinone (100 μm) reduced relaxations to exogenous NO by 54 ± 6%; this inhibition was partially reversed by Cu/Zn SOD (250 u ml−1), and by ascorbate (500 μm). Following inhibition of endogenous Cu/Zn SOD activity with diethyldithiocarbamate (DETCA), duroquinone (50 μm) also reduced relaxations to nitrergic field stimulation (by 53 ± 6%) and this effect was again reversed by Cu/Zn SOD and by ascorbate. Neither GSH (500 μm) nor α‐TOC (400 μm) afforded any protection against duroquinone.
- 3Xanthine (20 mu ml−1):xanthine oxidase (100 μm) inhibited NO‐induced relaxations by 73 ± 14%, but had no effect on those to nitrergic field stimulation, even after DETCA treatment. The inhibition of exogenous NO was reduced by Cu/Zn SOD (250 u ml−1) and ascorbate (400 μm), but was unaffected by GSH or α‐TOC (both 400 μm).
- 4Hydroquinone (100 μm) also inhibited relaxations to NO (by 52 ± 10%), but not nitrergic stimulation. In this case, however, the inhibition was reversed by GSH (5–100 μm) and ascorbate (100–400 μm), although Cu/Zn SOD and α‐TOC were ineffective.
- 52‐(4‐Carboxyphenyl)‐4,4,5,5,‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (carboxy‐PTIO, 50 μm) inhibited NO‐induced relaxations by 50 ± 4%, but had no effect on nitrergic responses; the inhibition was reduced by ascorbate (2–200 μm) and α‐TOC (10–200 μm), but not by Cu/Zn SOD or GSH.
- 6Hydroxocobalamin (5–1000 μm) inhibited, equally, relaxations to both NO (‐logIC40 3.14 ± 0.33) and nitrergic stimulation (‐logIC40 3.17 ± 0.22).
- 7Thus, a number of physiological antioxidants protected NO from superoxide anions, and from direct NO‐scavengers. The possibility that the presence of these antioxidants within nitrergically‐innervated tissues might explain the lack of effect of the NO inhibitors on nerve‐induced relaxation, without the need to invoke a transmitter other than free radical NO, is discussed.
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