Free radicals such as superoxide, hydroxyl
radicals, nitric oxide and peroxynitrite are very active chemical substances
that easily react with other molecules. They are very destructive like
cannonballs that indiscriminately cause protein deterioration, cell membrane
destruction, DNA damage, cell death and organ failure.
Dr. Takaaki Akaike and Dr. Hiroshi Maeda at the Department of Microbiology, Kumamoto University School of Medicine found that when laboratory mice were infected by influenza virus, the replication of the virus increased rapidly and peaked on day 4, then dropped down to baseline on day 8.
The lung consolidation scores (lung damage index) raised from day 2 and peaked on day 8 to day 10. Mice started to die from day 8 to day 14 (Akaike, Molla et al. 1989).
The activities of superoxide generator Xanthine Oxidase keep increased after the viral infection, and the superoxide (O₂⦁⁻) in the infected mice started to be generated from day 5 and reached to the peak on day 8.
In the meantime another important free radical, nitric oxide, peaked on day 8, were raised at the same time. It is therefore clear that a free radical storm occurred (Akaike, Ando et al. 1990) in the influenza virus infection.
Please note that inflammatory cytokine interferon gamma stimulated the generation of nitric oxide, as the antibody of interferon gamma suppressed such stimulation.
Simply by applying oxygen radical scavengers SOD (superoxide dismutase) or nitric oxide scavenger L-NMMA, the infected mice were protected and spared from death (Oda, Akaike et al. 1989);(Akaike, Noguchi et al. 1996).
These results explicitly tell us that free
radicals such as reactive oxygen radicals and nitric oxide are the immediate
life threatening factors in the virus induced pneumonia. The therapeutic
strategy should focus on preventing the damage caused by the over generated
free radicals, rather than targeting the virus itself.
Dr. Takaaki Akaike and Dr. Hiroshi Maeda at the Department of Microbiology, Kumamoto University School of Medicine found that when laboratory mice were infected by influenza virus, the replication of the virus increased rapidly and peaked on day 4, then dropped down to baseline on day 8.
The lung consolidation scores (lung damage index) raised from day 2 and peaked on day 8 to day 10. Mice started to die from day 8 to day 14 (Akaike, Molla et al. 1989).
The activities of superoxide generator Xanthine Oxidase keep increased after the viral infection, and the superoxide (O₂⦁⁻) in the infected mice started to be generated from day 5 and reached to the peak on day 8.
In the meantime another important free radical, nitric oxide, peaked on day 8, were raised at the same time. It is therefore clear that a free radical storm occurred (Akaike, Ando et al. 1990) in the influenza virus infection.
Simply by applying oxygen radical scavengers SOD (superoxide dismutase) or nitric oxide scavenger L-NMMA, the infected mice were protected and spared from death (Oda, Akaike et al. 1989);(Akaike, Noguchi et al. 1996).
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