[Microsomal hydroxylating system of the mouse liver in toxic forms of influenza infection]

Area of Science:

• Virology
• Biochemistry
• Toxicology

Background:

• Influenza A virus (H3N2) can cause toxic infections.
• Understanding the biochemical changes during viral toxicosis is crucial.

Purpose of the Study:

• To establish an experimental model of toxic influenza infection in CBA mice.
• To investigate the biochemical alterations associated with influenza virus toxicosis.

Main Methods:

• Induction of toxic influenza infection using A/Victory/35/72 (H3N2) strain in CBA mice.
• Electron spin resonance (ESR) technique to assess biochemical changes.
• Measurement of cytochrome P-450 content and p-nitroanisole o-demethylase activity.
• Analysis of lipid peroxidation (LP) and microviscosity in microsomes.
• Assessment of alpha-tocopherol levels.

Main Results:

• Viral toxicosis led to a decrease in active cytochrome P-450 content.
• Activity of p-nitroanisole o-demethylase was reduced during infection.
• Activation of lipid peroxidation (LP) was observed in microsomes.
• Increased microviscosity of the lipid matrix in microsomes was detected.
• Alpha-tocopherol content remained unchanged despite LP activation.

Conclusions:

• The experimental model effectively replicates toxic influenza infection in mice.
• Influenza virus toxicosis significantly impacts cellular redox balance and membrane properties.
• LP activation occurs independently of alpha-tocopherol levels in this model.