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The interaction between nitrogen oxides and hemoglobin and endothelium-derived relaxing factor
1Division of Environmental Health Research, Osaka Prefectural Institute of Public Health, Japan.
Free Radical Biology & Medicine
|January 1, 1989
Summary
Nitric oxide (NO) and nitrogen dioxide (NO2) are toxic nitrogen oxides with distinct biological effects. NO2 is an oxidant, while NO interacts with hemoglobin, impacting its function and leading to methemoglobin formation.
Area of Science:
- Biochemistry
- Toxicology
- Physiology
Background:
- Nitrogen oxides, including nitric oxide (NO) and nitrogen dioxide (NO2), are reactive free radicals with significant biological implications.
- NO2 acts as a potent oxidizing toxicant, whereas NO exhibits toxicity through interaction with hemoglobin, forming nitrosyl- and methemoglobin.
Purpose of the Study:
- To elucidate the toxicological mechanisms of NO and NO2, focusing on their interactions with hemoglobin and cellular components.
- To investigate the role of NO in physiological processes, such as endothelium-derived relaxing factors.
Main Methods:
- Electron spin resonance (ESR) spectroscopy was used to detect free radicals like nitrosylhemoglobin.
- Nitrate ion electrode was employed to establish reaction stoichiometry.
- In vitro assays assessed the effects of NO on methemoglobin reductase activity and nitrite-induced oxyhemoglobin oxidation.
Main Results:
- NO was observed to inhibit methemoglobin reductase activity.
- Nitrite was found to oxidize oxyhemoglobin autocatalytically, a process involving a free radical intermediate.
- The study identified aniline and aminopyrine as inhibitors of this autocatalysis, suggesting a radical-catalyzed conversion of nitrite to NO2.
Conclusions:
- NO and NO2 exert toxicity through distinct pathways involving hemoglobin interactions and oxidative stress.
- NO plays a role as an endothelium-derived relaxing factor, with its effects modulated by hemoglobin and superoxide dismutase.