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Biomedical subjects

P Bonnet

Publications and source records attributed to P Bonnet.

At least 127 records · Page 7Linked to original sources
PubMed1989

[In-vitro incorporation of BUDR by the prostate and by human urothelium and immunohistological detection in plastic-encased sections].

The measurement of the S phase fraction, essential parameter of cell proliferation, may be done through the immunohistochemical revelation of BUDR incorporated in the cells. The technique is illustrated. The advantages of in vitro incorporation as compared with in vivo injection as discussed. Easier than autoradiography, this method may be useful, in clinical practice, to study the aggressiveness of cancer tissues.

Bromodeoxyuridine↗
PubMed1988

Assessment of the relative hazard involved with airborne irritants with additional hepatotoxic or nephrotoxic properties in mice.

This paper deals with the conversion of the hepatotoxicity of 1,2-dichlorobenzene (DCB), the nephrotoxicity of hexachloro-1,3-butadiene (HCBD) and the respiratory effects of these two toxicants into quantal data. It aims to provide some useful information on the best strategy used for safety evaluation. A reflex bradypnea indicative of irritation of the nasal cavities of mice occurred during a 15-min oronasal exposure to each chemical. A reduction in the development of staining for liver glucose-6-phosphatase (G6-phosphatase) and an increase in the number of damaged tubules in cryostat kidney sections stained for alkaline phosphatase were the measure of toxicity in mice subjected to a whole-body 4-h exposure to DCB and HCBD vapours, respectively. The immediate irritant responses, as well as the delayed liver and kidney responses, were measured at the peak of the chemical's action. These maximum responses were then used to establish the relationships of exposure level effects and also the median active levels of exposure (MALs). The DCB and HCBD MALs responsible for a 50% decrease in the respiratory rate of mice (RD50) were 181 and 211 ppm, respectively. The MAL required for eliciting a 50% decrease in G6-phosphatase staining intensity in DCB-exposed mice was 598 ppm and that associated with 50% of damaged tubules in HCBD-exposed mice was 7.2 ppm. On the basis of these quantitative data, potency ratios indicated that irritation and kidney injury are the primary manifestations of toxicity associated with short-term exposure to DCB and HCBD, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1988

Toluene diisocyanate-induced airway hyperresponsiveness to intravenous acetylcholine: a study on single and repeated exposure in guinea-pigs.

We examined the changes in airway responsiveness to increasing doses of intravenous acetylcholine (ACh), in groups of 10 anaesthetized and tracheotomized spontaneously breathing guinea-pigs, 20 h after inhalation exposure to toluene diisocyanate (TDI). TDI exposure consisted of a single 4-h exposure to 1.2 ppm, intermittent exposures to 1.078 and 0.126 ppm for 4 h daily for 2 consecutive days, and continuous exposures to 0.118 ppm for 48 h or to 0.045 and 0.023 ppm for 1 week. Airway resistance (Raw) of the corresponding control groups, which inhaled clean filtered air, was used as baseline, and was similar for air and TDI groups. All the patterns of exposure, except exposure to 0.126 ppm TDI for 4 h daily for 2 consecutive days, significantly reduced by 28-60% the dose of ACh calculated to cause a 200% increase in Raw (ED200). The results indicate that TDI-induced airway hyperresponsiveness to ACh in guinea-pigs can occur at a level of exposure as low as 0.023 ppm for 1 week, and is consistent with the hypothesis of a cumulative effect.

Acetylcholine↗
PubMed1987

A programmed feedback control of solvent vapour concentrations in experimental inhalation chambers.

This paper describes a computer-controlled system to regulate solvent vapour concentrations in experimental inhalation devices. This system consists of an exposure chamber, a bubbler with a mass flow-meter, a monitor gas chromatograph and a computer. The frequency of automatic sampling was dependent upon the retention time of test materials. Flow-rate was corrected through a computer regulated bubbler as soon as the mean chamber concentration varied by more than 2.5% of a command level. Regulation coefficients were calculated by relating the concentration of vapours sampled with adsorbent tubes to the mean peak areas given by the monitor gas chromatograph. They were then fed into the computer allowing the actual concentration to be adjusted to the command level. Deliberately induced fluctuations in the level of acetone, ethanol and trichloroethylene, either sudden or progressive, were satisfactorily corrected as were fluctuations occurring normally during repeated exposures to ethanol. Variations were generally inferior to 5% of the command level.

Administration, Inhalation↗
PubMed1987

Intractable ascites in systemic mastocytosis treated by portal diversion.

A 50-year-old male presented with intractable ascites due to systemic mastocytosis. The diagnosis of systemic mastocytosis was established by histology of the bone marrow which showed mast cell infiltration and fibrosis. Ascites was related to portal hypertension which was documented by esophageal varices at endoscopy and by an increase of wedged-free hepatic venous pressure gradient. Liver biopsy disclosed dense fibrosis of hepatic arterial and portal venule walls, resulting in complete obstruction of some portal radicles. Peliosis hepatis and fibrous deposits in the walls of hepatic venules were also present. Because of intractable ascites and significant malnutrition, a portacaval shunt was performed which cleared ascites and dramatically improved the general condition of the patient.

Ascites↗
PubMed1987

Effect of SKF525-A on the glutathione-conjugating enzyme system and on liver toxicity.

SKF525-A given intraperitoneally (50 mg/kg body weight) to Sprague-Dawley rats in a single dose promoted a significant reduction in cytosolic glutathione S-transferase (GST) activities 0.5 and 1 h after injection. There was no decrease in liver non-protein sulfhydryls (NPSH) 0.5, 1 and 24 h after injection. Serum activities of glutamic pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), glutamic oxaloacetic transaminase (GOT) and glutamate dehydrogenase (GLDH) increased 1.8-, 2.9-, 3.8- and 41.2-fold respectively 8 h after injection, and the increased serum enzyme activities were maintained for up to 24 h. On the basis of these results, SKF525-A-induced blood manifestations of liver toxicity and decrease in GST activities may be regarded as confusing factors in the evaluation of the oxidative metabolism of compounds in Sprague-Dawley rats.

Alanine Transaminase↗
PubMed1987

Nasal and pulmonary toxicity of allyl glycidyl ether in mice.

A concentration-dependent expiratory bradypnea, indicative of irritation of the nasal mucosa, occurred during a 15-min oronasal exposure of mice to allyl glycidyl ether (AGE) in the concentration range of 1.9-8.6 ppm. The level of exposure responsible for a 50% decrease in the respiratory rate (RD50) was 5.7 ppm. Non-anaesthetized, tracheally cannulated mice exposed for 120 min to AGE at levels ranging from 105 to 185 ppm showed a concentration-dependent decrease in respiratory rate due to pulmonary toxicity. The level of exposure to AGE which produced a 50% decrease in the respiratory rate of tracheally cannulated mice (RD50TC) was 134 ppm. Mice were subjected to whole body exposure for 4, 9 or 14 days, 6 h/day to 7.1 or 2.5 ppm AGE. The 4-day exposure to 7.1 ppm AGE produced in the nasal cavities of mice lesions consisting of necrosis of the respiratory epithelium and complete erosion of the olfactory epithelium without pulmonary injury. Restorative responses were observed in the nasal cavities of mice exposed for 9 and 14 days to 7.1 ppm AGE. Exposure to 2.5 ppm AGE caused neither nasal nor pulmonary injury. The results indicate that AGE primarily affects the upper airways. They also make it questionable that the occupational standard of 5 ppm assures an adequate margin of protection against AGE-induced nasal effects.

Administration, Inhalation↗
PubMed1987

[Importance of the structure of the clot in thrombolysis].

Activation of plasminogen by tissue-type plasminogen activator (tpA) is potentiated by fibrin. We have demonstrated the role of fibrin polymerization in the potentiating effect of tpA-induced fibrinolysis. Therefore a pathogenic mechanism of thrombotic disorder may be related to an abnormal fibrin polymerization: the abnormal clot being less accessible to fibrinolysis than normal one. This defective lysis may be due to a defective enhancement by the abnormal fibrin of plasminogen activation by tpA, as demonstrated for fibrinogen Dusard, a congenital dysfibrinogenemia associated with a very severe thrombotic disorder. In some other cases, a decrease in the availability of the plasmin cleavage sites in fibrin clot may be involved. On the contrary, some antithrombotic drugs such as pentosane polysulfate in modifying clot structure allow a better degradation of fibrin clot by fibrinolytic enzymes. It is speculated that this enhanced fibrinolysis could explain, almost in part, the antithrombotic action of these drugs.

Blood Coagulation↗
PubMed1987

Extinction of mineralocorticoid effects in 19-norprogesterone derivatives: structure-activity relationships.

19-Norprogesterone (19-NOR-P) is a potent progestagen in mammals by s.c. injection, but is almost inactive when given p.o. In the rat, 19-NOR-P also shows marked salt-retaining and hypertensive effects, consistent with its high affinity for mineralocorticoid receptors (MR). We synthetized recently some p.o. active 19-NOR-P derivatives, and have examined the extent to which the structural changes made on the parent compound can modify the affinity for MR and the salt-retaining potency. Compared with aldosterone, 19-NOR-P has a 47% affinity for rat renal cytosolic MR, decreasing to 13% with alpha-hydroxylation on C-17 (17 alpha-OH-19-NOR-P). The addition of a methyl group combined with the formation of a double bond at C-6 led to nomegestrol, the relative affinity of which was 1.2%. Binding was almost abolished completely (0.23%) by acetylation of the 17 alpha-OH group (nomegestrol-acetate). A single s.c. injection of 19-NOR-P, 20 micrograms/animal, induced a marked decline of [Na+]/[K+] ratio in urine of adrenalectomized male rats. The antinatriuretic effect was still observed after a 11-day period of daily administrations of the same dosage. 17 alpha-OH-19-NOR-P decreased the [Na+]/[K+] ratio only at a high p.o. dose (2500 micrograms/animal). NOM-Ac did not affect the [Na+]/[K+] ratio after a single s.c. or p.o. administration, but increased it at the end of a 11-day p.o. treatment. Thus, the chemical modifications that lead to potent p.o. active progestins derived from 19-NOR-P induce stepwise reductions in the affinity for MR and of the mineralocorticoid effects of the parent compound.

Adrenalectomy↗