Biomedical subjects
Publications and source records attributed to F Marcucci.
Cyclic AMP and cyclic GMP phosphodiesterase activity was determined in the heart and in nine skeletal muscles of control and dystrophic Re 129/J male and female mice. Phosphodiesterase activity in the presence of 0.5 mM cyclic AMP of cyclic GMP was increased in all the muscle but the heart of dystrophic mice.
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1, 5 and 10 mg/kg vinyl chloride monomer (VCM) in aqueous solution were injected i.v. into male rats with cannulated tracheas. Respiratory activity was regulated to permit investigation of the effect of modifying pulmonary ventilation on VCM excretion in blood and expired air assayed at different intervals for VCM. VCM excretion rate was found to be directly proportionate to pulmonary ventilation. When respiration was stopped for 1 min after VCM injection, there was no decrease in blood BCM, the main route of elimination of i.v. injected VCM thus being pulmonary.
The effects of chronic di-(2-ethylhexyl)phthalate (DEHP) on liver microsomal activity were studied in rats. Daily doses of 50 and 500 mg/kg for 4 weeks did not affect O-demethylation, aromatic hydroxylation, N-demethylation, C3-hydroxylation, styrene monooxygenase, glutamic-oxalacetic and glutamic-pyruvic transaminases (GOT, GPT). Inhibition of glutathione-S-transferase A and C and induction of epoxide hydrase, glutathione-S-transferase B and nitroreductase activity were instead observed. Protein, cytochrome P-450 and reduced glutathione levels in liver did not appear to be affected by DEHP pretreatment.
We have investigated the proliferative response and interferon production in cultures of mouse thymocytes stimulated with two different mitogens, PHA (phytohemagglutinin), or Con A (concanavalin A). Normal thymocytes proliferated weakly and did not produce detectable interferon levels in response to both mitogens. Supplementing this cell population with macrophages or adding 2-mercaptoethanol to the culture medium strongly enhanced the proliferative response to both mitogens, but only in response to PHA marginal levels of interferon could be detected. When the steroid-resistant population was tested, both PHA and Con A induced strong proliferative responses; in this case significant interferon levels could be obtained after stimulation with PHA, but only borderline levels with Con A. Peripheral lymphocytes from the spleen responded identically to both mitogens with respect to interferon production as well as proliferation. The data suggest that distinct differentiation pathways may exist for T lymphocytes producing interferon in response to different mitogens.
5 healthy volunteers (3 males, 2 females, aged 22-35 years) were given 600 mg ditazole (Ageroplas) every 12 h (9.00 a.m. and 9.00 p.m.) for 10 days. Venous blood was collected from all volunteers at 9.00 and 11.00 a.m. on days 0, 3, 5, 7 and 10. The threshold concentrations of adrenaline inducing two distinct waves of platelet aggregation (Born's method) within 3 min were determined each time. Blood levels of ditazole were measured by a gas-chromatographic technique using a nitrogen-phosphorus selective detector. The average blood levels of the drug ranged between 0.84 and 1.30 microgram/ml at 9.00 a.m., and between 1.93 and 2.85 microgram/ml at 11.00 a.m. Inhibition of platelet aggregation (expressed by a grading system in arbitrary units) ranged between 1.6 and 2.0 at 9.00 a.m. and between 2.0 and 2.4 at 11.00 a.m. The fluctuations of blood levels and platelet aggregation inhibitory activity of ditazole observed during the study period were virtually the same. It is suggested that the treatment schedule used in the present study results in blood levels of ditazole sufficient to reveal any consistent alteration of platelet function in normal subjects.
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To challenge the hypothesis that interferon (IF) production in chronic hepatitis-B virus liver disease is defective, lymphocytes from 14 patients with chronic active liver disease (CALD); from nine patients with chronic inactive liver disease (CILD), and from six healthy chronic carriers (HCC) were stimulated by Newcastle Disease virus. The patients with CILD showed a weak IF response by comparison with the controls (P less than 0.0005), whereas IF production by CALD patients and the HCC did not statistically differ from IF production in the healthy hepatitis-B surface antigen negative subjects who served as controls. These results indicate that IF treatment of CALD does not rely on a completely proved background.
1. A method for measuring vinyl chloride monomer (VCM) concn. in rat blood and tissues is described, using a head-space g.l.c. technique with flame ionization detector. The method is sensitive to 5 ng/ml VCM in blood and 30 ng/g in tissues. 2. VCM disposition was determined in rat blood, liver, kidney, brain and lung at different intervals after administration of 1--10 mg VCM/kg i.v. and 10 mg/kg orally. 3. VCM distributed rapidly in the organism after i.v. administration; it was eliminated rapidly and was no longer detectable at 15 min for the highest dose and at 4 min for the lowest. VCM was absorbed rapidly when given orally and tissue concn. were measurable for longer than after i.v. treatment. For both routes, VCM concn. in liver and lung decrease faster than in other organs, suggesting that these organs play a role in VCM elimination.
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The distribution of ditazole in blood and tissues of rats was determined by a simple GLC technique. Ditazole, after intravenous injection in rats (20 mg/kg), entered preferentially into the brain, the liver, and the heart in decreasing order. In the epididymal adipose tissue, the drug was present only in small amounts. Ditazole disappeared from the rat organs 4 hr after the treatment. The apparent ditazole half-life in rat blood was 41 min, the volume of distribution was 2.068 liters/kg, and the body clearance was 0.0345 liter/kg/min.
Camazepam, 5 mg/kg iv, was injected in rats and mice to study its distribution in the blood and brain. Peak blood levels were about 0.9 microgram/ml in rats and 0.6 microgram/ml in mice. Peak brain levels were about 1.5 microgram/g in rats and 0.8 microgram/g in mice. The apparent blood half-life of camazepam was 9 min in mice and 20 min in rats.
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Three structurally related benzodiazepines were studied as substrates for hydroxylation by liver microsomal enzymes of rats and mice. The Vmax was comparable for dechlorodesmethyldiazepam, desmethyldiazepam, and 2'-chlorodesmethyldiazepam in the two animal species. The apparent Km decreased from dechlorodesmethyldiazepam to 2'-chlorodesmethyldiazepam for liver microsomal enzymes from both animal species. The hydroxylation of desmethyldiazepam and 2'-chlorodesmethyldiazepam yielded two pharmacologically active metabolites, oxazepam and lorazepam, respectively.