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  • 1
    ISSN: 1432-1238
    Keywords: Key words Nitric oxide ; Methemoglobin ; Methemoglobinemia ; Adverse effects ; Ascorbic acid ; Glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The objective of the present study was to investigate the treatment of nitric oxide (NO)-induced methemoglobinemia by ascorbate and its consequences on red blood cell (RBC) glutathione in vitro. RBC were obtained from five healthy volunteers. The following experiments were carried out: (1) After methemoglobin generation by NO, ascorbate was added (2) RBC were simultaneously exposed to NO and ascorbate (3) Methemoglobin was generated by NO, ascorbate was added and incubation with NO continued. (1) After discontinuation of NO, the mean half life for methemoglobin was reduced from 195 min (controls) to 60 min (10 mM ascorbate) in a dose-dependent manner. (2) Methemoglobin formation after 3 h of NO exposure was 2.7 ± 0.3 % in controls and 1.8 ± 0.1 % with 10 mM ascorbate (p 〈 0.01). (3) Further methemoglobin formation was inhibited only by 10 mM ascorbate (p 〈 0.001). NO incubation did not affect RBC glutathione (86.5 ± 19.6 and 86.5 ± 19.6 mg/l, respectively). Treatment with 10 mM ascorbate significantly decreased glutathione (p 〈 0.002). In vitro, NO-induced methemoglobin formation is significantly decreased only by a high (10 mM) ascorbate concentration. Glutathione, critical for ascorbate activity, is not influenced by NO.
    Type of Medium: Electronic Resource
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