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Biomedical subjects

B Pipy

Publications and source records attributed to B Pipy.

At least 73 records · Page 4Linked to original sources
PubMed1989

Lipid peroxidation in rat liver microsomes: influence of carcinogenic N-nitrosocarbaryl.

The reactivities of carbaryl, N-methyl 1-naphthylcarbamate insecticide and its N-nitrosated derivative carcinogenic, N-nitrosocarbaryl, were investigated on the microsomal hepatic lipid peroxidation and NADPH-dependent reductase activities. The in vivo treatment by N-nitrosocarbaryl produced a reduction in lipoperoxidative degradation induced in vitro by NADPH with regard to the formation of malonaldehyde and conjugated dienes. Carbaryl, its precursor did not affect lipid peroxidation under the same in vivo conditions. Moreover, following administration of the 2 compounds, the activities of NADPH-cytochrome c reductase as well as NADPH-neotetrazolium reductase were significantly decreased by N-nitrosocarbaryl but not influenced by carbaryl. Correspondingly, in vitro studies were performed; different action patterns of the 2 tested xenobiotics were also noted after treatment of rat liver microsomes in vitro by carbaryl and N-nitrosocarbaryl especially in their ability to cope with microsomal oxygen activation. N-Nitrosocarbaryl proved to have a potent inhibitor concentration effect on NADPH-dependent chemiluminescence response in vitro; carbaryl was virtually ineffective on this parameter. No significant difference appeared in the affinity of N-nitrosocarbaryl and carbaryl for the microsomal phospholipids. From the in vitro explorations, it was suggested that carcinogenic N-nitrosocarbaryl may be involved in the inhibition mechanism of microsomal lipid peroxidation through decreases in both NADPH-dependent reductase activities and superoxide generation.

Alkylating Agents↗
PubMed1989

Interaction of carbaryl and N-nitrosocarbaryl with microsomal monooxygenase activities.

The in vitro interactions of carbaryl and carcinogenic N-nitrosocarbaryl with rat liver microsomal monooxygenase activities are compared. The inhibitory effect of the nitroso-compound is demonstrated to be non-competitive on aminopyrine N-demethylase, p-nitroanisole O-demethylase and aniline hydroxylase. The nature of the inhibition induced by the parent amide is found to be competitive on aminopyrine N-demethylase and p-nitroanisole O-demethylase. Correspondingly, in vitro studies of the metabolism of the two compounds were carried out: they both yield formaldehyde. Moreover, N-nitrosocarbaryl is denitrosated through a NO-cytochrome P-450 complex during microsomal metabolism. The toxic effects and biological activities of the two compounds are discussed on the basis of data of metabolic studies and different patterns of enzyme inhibition.

Animals↗
PubMed1989

In vitro influence of molybdenum on benzo[a]pyrene metabolism in hepatic and pulmonary rat microsomes.

Our study presents the in vitro molybdenum influence on benzo[a]pyrene (BaP) microsomal metabolism. Addition of various concentrations of different molybdenum salts [MoS2, MoCl5, (NH4)6Mo7O24 . 4H2O] to liver and lung microsomal fractions of rats previously treated with 3-methylcholanthrene produces a decrease in the different BaP metabolites assessed by high-performance liquid chromatography (HPLC) analysis. This inhibition varies, depending on the considered metabolite and in relation to both the molybdenum level and the origin of the microsomal suspension. The minimum effective concentration is 0.26 and 0.52 mM Mo from liver and lung, respectively. The inhibitory potencies of the +5 (chloride) and +6 (ammonium heptamolybdate) molybdenum compounds are comparable; that of the sulfide is lower.

Animals↗
PubMed1989

[Immunopharmacologic study in mice of 2 beta-1, 3, beta-1, 6 polysaccharides (scleroglucan and PSAT) on the activation of macrophages and T lymphocytes].

The immunopotentiating activity and mechanisms of PSAT and scleroglucan, two beta 1-3, beta 1-6 glucan, were investigated in mice: these polysaccharides increase the chemiluminescence of peritoneal phagocytes and the serum C3 level. Augmentation of DNA synthesis of spleen cells was induced in vivo by injecting PSAT or scleroglucan. An additional proliferative effect of these polysaccharides was observed when spleen cells were incubated with mitogens. Moreover, PSAT enhances the number of Thy1 lymphocytes and increases the ratio of lymphocytes L3T4/Lyt2 in mice infected with Toxoplasma gondii. No significant changes in immunoglobulin levels were found. These data indicate that PSAT and scleroglucan favorably affect the non-specific host defense and cellular immune response in mice.

Animals↗
PubMed1988

Patulin immunotoxicology: effect on phagocyte activation and the cellular and humoral immune system of mice and rabbits.

Patulin is a mycotoxin frequently found in rotten apples or molded corn. We have investigated the effect of sublethal doses of patulin on the immune system in mice and rabbits. A significant suppression of the chemiluminescence response of peritoneal leucocytes was observed in both species. Mouse spleen lymphocytes showed a decrease in absolute number, most pronounced for the B-cell population whereas the Ts population showed a relative increase after patulin treatment. The mitogenic response to PHA, Con A and, in particular, PWM was also depressed by patulin. This was paralleled by decreasing serum immunoglobulin levels in the mice and rabbits. The immunosuppressive effect of patulin is reversible and is probably due to interaction with cellular free SH groups since the action of patulin can be circumvented, at least partially, by the prior administration of cystein. Under natural circumstances, patulin may constitute a health risk for animals.

Animals↗
PubMed1988

[Enhancement of resistance of mice Toxoplasma gondii by 2 polysaccharides beta 1-3, beta 1-6 (PSAT and Scleroglucan)].

The protective effect of PSAT and Scleroglucan (beta 1-3, beta 1-6 polysaccharides), has been studied in mice infected with different strains of Toxoplasma gondii (RH, attenuated RH or Prugniaud strains). Intramuscular or intravenous administration of PSAT before infection of mice by the attenuated RH strain, resulted in a significant enhancement of survival: 100% of survival in the treated group, compared to 33% in controls and 50% in mice pretreated with Scleroglucan (10 mg/kg, intravenously). In contrast, there was no difference in the survival rate between the group treated with PSAT (1 mg/kg, IV) and the control in mice infected with the virulent RH strain: all mice died between day 7 and day 8. In mice infected with 15 cysts of the Prugniaud strain a decrease in the chemiluminescence (CL) of peritoneal macrophages and of the number of cysts in the brain of mice were observed in mice treated either with PSAT (1 mg/kg, IM) or scleroglucan (10 mg/kg, IM).

Adjuvants, Immunologic↗
PubMed1986

The effect of carbaryl on the arachidonic acid metabolism and superoxide production by mouse resident peritoneal macrophages challenged by zymosan.

Carbaryl, a broad spectrum insecticide with anticholinesterase activity, was tested for its ability to disturb resident peritoneal macrophages stimulated by opsonized zymosan. The effect of carbaryl on superoxide production and on the release of [1-14C] arachidonic acid and 14C-labelled prostaglandins was dose-dependent. For 2.5 X 10(-6) M of carbaryl, superoxide production and prostaglandin release were not significantly inhibited. At 12.5 X 10(-6) M, the inhibitory effect was apparent for superoxide production (33%) and for the release of 6 KPGF1 alpha (60%), PGE2 (42%), PGF2 alpha (38%), PGD2 (33%). Carbaryl had no effect on the level of free arachidonic acid. Insecticide at 12.5 X 10(-6) M significantly decreased the deacylation of the phosphatidylcholine (20%). Incubation of resident peritoneal macrophages with indomethacin studied conjointly decreased only the prostaglandin release. These results suggest that carbaryl decreases the sequence of events following the binding of a particulate agent to its receptor and leading to the induction of phospholipase activity and the subsequent release of 20:4 and the oxidative burst in the cells. The effect of this pesticide on phospholipid metabolism and its consequences on macrophage stimulation are discussed. Ecto-serine esterase inhibition in the effect mechanism of the pesticide was suggested.

Animals↗
PubMed1985

[1-14C]Arachidonic acid incorporation into glycerolipids and prostaglandin synthesis in peritoneal macrophages: effect of chloramphenicol.

Peritoneal macrophages from normal mice were labelled with [1-14C]arachidonic acid after 2 h culture. The uptake of arachidonic acid into cellular lipids was rapid, time-dependent and can be represented within the limit of the studied times by a parabolic regression. Indomethacin decreased the kinetics of uptake; this inhibition is dose-dependent. Chloramphenicol had no effect on macrophage [1-14C]arachidonic acid uptake. After 3 h, the radioactivity was recovered in phosphatidylcholine (38.6%), phosphatidylserine-phosphatidylinositol (8.5%), phosphatidylethanolamine (22.1%), diacylglycerol (2.9%), triacyglycerol (2%) and cholesteryl ester (11.8%). Chloramphenicol and indomethacin inhibited the labelling of phospholipids and stimulated the labelling of neutral lipids and cholesteryl ester. Studies on arachidonic acid release from glycerolipids of prelabelled 2-h cultured macrophages showed that phosphatidylcholine and phosphatidylserine-phosphatidylinositol are the major source of arachidonic acid in prostaglandin synthesis in macrophages stimulated or not by zymosan. Chloramphenicol inhibited release of fatty acid from phosphatidylcholine and phosphatidylserine-phosphatidylinositol; indomethacin had no effect. Both drugs inhibited prostaglandin synthesis in stimulated or non-stimulated macrophages. In the culture medium, indomethacin increased the release of free arachidonic acid by stimulated macrophages. Possible explanations for the mechanisms underlying these effects are presented. It is concluded that indomethacin and chloramphenicol exert profound effects on the metabolism of phospholipids and its zymosan activation. Chloramphenicol appears to impair prostaglandin synthesis through several mechanisms and especially through phospholipase inhibition.

Animals↗
PubMed1984

The effects of locally injected antibiotic on carrageenan-induced granuloma in rats.

Indomethacin (0.5 mg/100 g b.w./day) and chloramphenicol (0.5 mg or 15 mg/100 g b.w./day) were tested for their anti-inflammatory effects on 7th day carrageenan-induced granuloma formation. Neither of the drugs modified granuloma or pouch wall weight but they decreased the exudate and the cluster of dead cells. Indomethacin and chloramphenicol decreased glucosamine in the dead cell granuloma fraction and increased the level of collagen in the pouch wall. The drugs differed in their inhibitory effect on lysozyme and prostaglandin E2 accumulation in the exudate. The increase in collagen was related to a drop in the level of prostaglandin E2 which seems to regulate collagen deposition in the granuloma. However, the prostaglandin E2-lysozyme correlation--which was only significant with chloramphenicol--suggests a mode of action for chloramphenicol different from that of indomethacin. Chloramphenicol could act by a myelodepressive and/or chemotactic effect. The effects of chloramphenicol on the macrophages are discussed.

Animals↗
PubMed1983

Evaluation of cellular and humoral mechanisms of carbaryl-induced reticuloendothelial phagocytic depression.

The simultaneous injection of carbaryl and colloidal carbon phagocytized by the reticuloendothelial cells results in competition between the two substances in favor of the carbon particles. Experiments with opsonized carbaryl suggest that the decrease in carbaryl blood clearance by the colloid is mediated by a depletion of serum opsonins. Following blockade, the liver carbaryl uptake was depressed in the control group (17%), while it was increased in the opsonized group (12%). With all preparations of carbaryl, opsonized or non-opsonized, colloidal carbon produced a slight and variable increase in carbaryl uptake by the spleen and lungs. These results indicate that, besides the uptake of carbaryl by the hepatocytes, other clearance sites must also be considered such as the Kupffer cells and other liver sinusoidal cells. Moreover our results show that intravenous administration of carbaryl induces a state of phagocytic depression as indicated by impaired intravascular phagocytosis and depressed hepatic uptake of the reticuloendothelial (RE)-test colloidal suspension. The results obtained from injection of opsonized colloidal particles during carbaryl-induced RE-depression, and the fact that carbaryl and carbon are both opsonized by the same serum factor, suggest that the mechanisms of RE-blockade involve selective hepatic and splenic macrophage failure and depletion of serum opsonins. According to our enzymatic investigation, this failure of the RE system to incorporate colloids during carbaryl--RE-blockade could be due to a defect in the activity of macrophage membrane-bound serine esterase.

Animals↗
PubMed1981

Distribution of radioactivity following oral administration of carcinogenic 14CH3-labelled nitrosocarbaryl in the rat.

After a single intragastric administration of 14C-labelled carcinogenic nitrosocarbaryl, a nitrosated pesticide, the distribution of radioactivity was investigated in the blood and a number of organs in male rats. The animals received 0.25 mg/kg of labelled nitrosamine and were killed following administration at timed intervals between 0.5 h and 24 h. Our results show that the greatest amount of the 14CH3--group was associated with the forestomach, tumor-susceptible tissue; the level of radioactivity is noteworthy but less important in the glandular stomach. There are also sites of radioactivity accumulation mainly in the liver. Moreover, [14C]nitrosocarbaryl was revealed in the blood suggesting that nitrosamine itself rapidly (0.5 h) crosses the intestinal barrier and in a significant quantity (13%). These facts constitute a potential carcinogenic risk.

Animals↗
PubMed1980

Phagocytic activity of the rat reticuloendothelial system and the pharmacokinetics of an anticholinesterasic insecticide: carbaryl.

1. The pharmacokinetics of [14C]carbaryl administered intravenously and orally were studied in male rats whose reticuloendothelial system (RES) was inhibited by colloidal carbon or activated by glyceryl trioleate. 2. A time course for [14C]carbaryl blood concn. was fitted to a two-compartment open model following single intravenous administration. A single exponential decay was noted following intragastric administration. 3. The constant blood elimination of [14C]carbaryl decreased significantly in animals with the RES inhibited and increased in those whose RES was activated compared to control animals. 4. There was an increase in carbaryl concn. in the tissue compartment in animals with the RES activated, but no change in animals with the RES inhibited. 5. The equivalent [14C]carbaryl concn. of liver and lungs were decreased or increased in animals with the RES inhibited or activated respectively.

Animals↗
PubMed1979

Effect of blockade of the reticuloendothelial system on the carbaryl toxicity in the rat.

The time dependence of the level of blood cholinesterase was determined in rats with the reticulo-endothelial system (RES) inhibited with colloidal carbon and in control rats after i.v. administration of 2 does of carbaryl: 0.75 mg and 1.50 mg/100 g body wt. Pretreatment with colloidal carbon had no effect on the blood cholinesterase activity when compared with the controls. Carbaryl rapidly inhibits cholinesterase; the time of "reactivation" of this enzyme increases with the administered dose. However, when the RES is inhibited with colloidal carbon, "reactivation" of cholinesterase is significantly slowed down, to a varying degree, depending on the dose of carbaryl. Our results bring to light a relationship between the inhibition of the RES and the toxicity of carbaryl, inhibition increasing the anticholinesterase effect of the insecticide.

Animals↗
PubMed1978

[Effect of blockade or stimulation of the reticuloendothelial system on the blood clearance kinetics of the anticholinesterase insecticide carbaryl in the rat].

The blood clearances of 14C-carbaryl and colloïdal carbon were studied in Rats with reticuloendothelial system (RES) inhibited or activated, and in control Rats. A correlation was established between the blood clearance kinetics of carbon particles and carbaryl; such data support the concept of the contribution of the RES in the disappearance of carbaryl from the circulation.

Animals↗
PubMed1978

[Phagocytic activity of the reticuloendothelial system in the rat after administration of an anticholinesterasic pesticide, carbaryl (author's transl)].

The effects of 4 carbaryl doses (0.375, 0.75, 1.50 and 3 mg/100 g) on the reticuloendothelial system (RES) phagocytic activity were studied 1 h after their administration to male rats. Carbaryl reduced RES phagocytic activity. Results showed a dose-dependent drop in RES phagocytic activity. Carbaryl might act as an inhibitor of phagocytes by saturing them to greater or lesser degree, depending on the dose administered.

Animals↗