Effects of rutin and quercetin on monooxygenase activities in experimental influenza virus infection.

The aim of this work is to study the effect of the flavonoids rutin and quercetin on hepatic monooxygenase activities in experimental influenza virus infection (EIVI). EIVI causes oxidative stress in the whole organism. This is confirmed by the rapidly increased concentrations of thiobarbituric reactive substances in influenza-infected mice: lungs - 290%; blood plasma - more than 320%; liver - 230%; brain - 50%.

Effect of vitamin E and vitamin C combination on experimental influenza virus infection.

Successful antioxidant treatment of the so-called "free radical diseases" has been reported in the literature. In this study we examined the preventive effect of vitamin E and vitamin C, alone and in combination, on the damage caused by influenza virus infection (IVI). Male mice (ICR), infected with influenza virus A/2/68/(H3N2) (1.

Antioxidant properties of rimantadine in influenza virus infected mice and in some model systems.

Influenza virus infection is associated with development of oxidative stress in lung and blood plasma, viz. increase of primary and secondary lipid peroxidation products. It was established that rimantadine treatment led to a decrease of the products of lipid peroxidation in tissues of mice experimentally infected with influenza virus A/Aichi/2/68 (H3N2).

Interaction of dexamethasone with acetylsalicylic acid in mice.

The effect of acetylsalicylic acid (ASA, 160 mg/kg b.wt.) and dexamethasone (DEX, 15 mg/kg b.

Influence of hydrocortisone on the analgesic effect, toxicity and metabolism of aspirin in mice.

1. Hydrocortisone (HC; 80 mg/kg body weight, intraperitoneally for 4 days), both alone and in combination with acetylsalicylic acid (ASA; 160 mg/kg body weight, orally, for 4 days), decreased ASA general and specific toxicity via metabolic modulation of drug-metabolizing enzyme systems (intestinal ASA-esterase and hepatic UDP-glucuronyltransferase) and did not change the ASA analgesic effect. 2.

Toxicity and enzyme-inducing effect of the antiviral compound mopyridone in mice.

Mopyridone (CAS 82822-14-8, MP) is a new antiviral compound with low acute toxicity in mice. Phenobarbital (PB) induction did not alter MP oral acute toxicity, while methylcholanthrene (MC) and dexamethasone (DEX) induction increased it. MP (1/10 of LD50, 5 days) increased aniline hydroxylase activity (by 158%) and cytochrome P-450 content (by 43%), but has no significant effect on liver N-demethylase activity (ethylmorphine N-demethylase, amidopyrine N-demethylase and benzphetamine N-demethylase) in mouse liver 10,000 x g supernatant.

Effects of acetysal, dexamethasone and their combination on drug metabolizing enzyme systems in rat liver microsomes.

After 4 days of acetysal treatment (160 mg/kg body weight orally), the following were established: a higher acute toxicity of acetysal, an inducing effect on amidopyrin N-demethylase and analgin N-demethylase activity and increases in cytochrome P-450 and cytochrome b5 content. Aniline hydroxylase activity decreased, thiopental sleeping time was prolonged and UDP-glucuronyltransferase activity was not changed. Dexamethasone, at a dose of 5 mg/kg body weight p.

Acute toxicity and effects on hepatic oxidative drug metabolism of mopyridone.

Mopyridone (CAS 82822-14-8) is a new chemotherapeutic with a strong antiviral effect (vs. influenza- and toga viruses) and certain advantages over the chemotherapeutics known so far. Toxicological studies reveal its low oral and intraperitoneal toxicity in mice and rats.

Effect of desoxycorticosterone on the activity of drug-metabolizing enzyme systems.

Single administration of desoxycorticosterone acetate (DOCA) in a dose of 50 mg/kg body mass intramuscularly in male Wistar rats revealed dose-dependent potentiation of hexobarbital sleeping time and inhibition of the activity of the oxidases with mixed functions in substrates of types I (hexobarbital, ethylmorphine) and II (aniline), although this is not accompanied by changes in the components of the electron-transport chain. It is assumed that DOCA may possibly inhibit the metabolism of the above mentioned substrates, being an alternative substrate of oxidases with mixed functions. In an acute experiment DOCA does not influence the activity of esterases (liver esterase A and intestinal esterase B), but the compound has an inhibitory effect on some synthetase reactions--cytosol glutathione-S-transferase.