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Biomedical subjects

R Derache

Publications and source records attributed to R Derache.

At least 19 recordsLinked to original sources
PubMed1985

Nutritional and toxicological effects of long-term ingestion of phosphine-fumigated diet by the rat.

The fumigation of stored foodstuffs with phosphine (PH3) is likely to become widely used in the future because of its technological efficiency and the rapid desorption of the fumigant. In a long-term feeding study of a phosphine-fumigated diet, rats were monitored for weight gain, food intake, plasma chemistry, haematology and urinary changes. Histopathological studies, including organ-weight determinations, were carried out after treatment of the rats for 1 and 2 yr. The results show that ingestion of a phosphine-fumigated diet by the rat for 2 yr does not cause any marked modification of growth, food intake, nitrogen balance, body composition, functional behaviour or the incidence or type of tumours.

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

[Effects of oxythioquinox on urinary nitrogen excretion in rats].

The amount of nitrogen excreted in urines is higher in pair-fed Rats subjected to a diet containing 400 mg/kg of oxythioquinox. This is a consequence of specific effect of oxythioquinox on protein catabolism and not to a renal failure as is shown by the increase in the urinary excretion of urea. The administration of vitamin B6, B12 and folic acid improves the growth but these vitamins have no effect on the nature of urinary nitrogen excretion.

Animals↗
PubMed1982

[Effect of preincubation of hepatic microsomes in the presence of chloramphenicol on microsomal lipid peroxidation].

The influence of anaerobic preincubation of hepatic microsomes in the presence of chloramphenicol, in the view of reduction of nitro-group has been studied on later peroxidative degradation and activity of several enzymatic systems on lipids of pretreated microsomes. An inhibition of malonaldehyde production and conjugated dienes occurs in these conditions. Activity of methylaniline N-demethylase and Neotetrazolium reductase were not affected. Possible relationships of chloramphenicol and its reduced metabolites on lipoperoxidation are discussed.

Anaerobiosis↗
PubMed1982

Effects of polychlorinated biphenyls on liver regeneration in the rat: influence of position and degree of chlorination.

The effects of PCBs, administered intragastrically, were studied on partially hepatectomized (70%) rats. Seven days after hepatectomy, a relationship was noted between the increase in the degree of chlorination of the biphenyl molecule and the hypertrophy and lipid accumulation in the liver. When the 3' and 4' positions are chlorinated, the relationship still holds but, for a constant number of chlorine atoms, the intensity of the effects are decreased. Fourteen days after hepatectomy, there was only a significant difference in the case of decachlorobiphenyl and Phenoclor DP5, for which the hypertrophy is accompanied by hyperplasia. The relationships are discussed between the chemical structure of the PCBs, their metabolization, their toxicity, and the reversibility of their effects.

Animals↗
PubMed1981

Evaluation of the toxic risk of DDT in the rat: during accumulation.

An investigation was undertaken on the accumulation of DDT and its metabolites in the rat. Rats received 14.5 mg DDT/kg b.w. every day for 52 days. Growth, food intake, body composition, and the activities of various enzymes were little affected. However, the level of total lipids fell 30% and the weight of the liver rose 20% due to cellular hypertrophy induced by the DDT. The quantity of DDT and its metabolites found in the carcass was 24 mg/rat i.e. three times that found in rats dead after a single dose of 200 mg/kg. Liver and brain contained 130 micrograms/rat and 10 micrograms/rat, respectively i.e. five times lower than those found in the rats which died from an acute dose of DDT. In the carcass, p,p' DDT accumulates more than p,p' DDE or p,p' DDD; the latter is preponderant in the liver.

Analysis of Variance↗
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↗
PubMed1981

[Hepatic microsomal monoxygenase inhibition by nabam in the rat (author's transl)].

Nabam (fungicide dithiocarbamate) has been incorporated with the diet of rats during six months (the doses were: 0, 10, 50, 100, 500, 1000 and 2000 ppm). It decreases significantly the hepatic microsomal enzymes activity (aniline hydroxylase and aminopyrine N-demethylase and the liver P 450 content, but the cytochrome b 5 concentration doesn't seem to be modified. The microsomal lipidic and proteic content is only modified with the highest Nabam dose. Several hypotheses may be proposed to explain the Nabam effects: one is the inhibition of the monooxygenases and their biosynthesis repression.

Aminopyrine N-Demethylase↗
PubMed1980

Foetal and maternal rat brain acetylcholinesterase: isoenzymes changes following insecticidal carbamate derivatives poisoning.

Pregnant rats (18th day) were orally given insecticidal carbamates with anticholinesterasic properties: 50 mg/kg carbaryl, 0.1 mg/kg aldicarb, 2.5 mg/kg carbofuran and 20 mg/kg pirimicarb. The acetylcholinesterase (AChE) isoenzymes from the brain of mothers and their foetuses were separated by electrophoresis on polyacrylamide ge. The four carbamate derivatives caused a significant lowering of the percentage of the least mobile isoenzyme (isoenzyme 1) in mother. Aldicarb, carbaryl and pirimicarb also caused a significant decrease in the percentage of the first foetal isoenzyme. The second foetal isoenzyme underwent a decrease after treatment with aldicarb or carbofuran. The distribution of the foetal isoenzymes was seen to be different to that of the dams in both control and treated animals. The difference in sensitivity of the cerebral AChE to the insecticides under investigation is thought to depend on differences of the fixation of carbamate derivatives on the foetal and maternal isoenzymes.

Acetylcholinesterase↗
PubMed1980

Inhibition of two rat hepatic microsomal drug-metabolizing enzymes by a carcinogenic N-nitrosated pesticide: N-nitrosocarbaryl.

N-Nitrosocarbaryl (N-methyl-1-naphthyl N-nitrosocarbamate) was intraperitoneally administered to male and female rats on four consecutive days at the following doses: 6.25 mg, 12.5 mg, 25 mg and 50 mg/kg body weight/day in olive oil solution; the controls received just the oil. In a second experiment, a daily intraperitoneal dose of 25 mg/kg of N-nitrosocarbaryl was given for 1, 2, 3 or 4 days; the animals were killed 24 h after the last treatment. The two following microsomal enzymatic activities were assayed: aniline aromatic hydroxylase and p-nitroanisole O-demethylase; the levels of cytochrome P-450, proteins and RNA were measured in the hepatic microsomal fraction. N-Nitrosocarbaryl is an inhibitor of the two investigated microsomal monooxygenases at doses of 25 and 50 mg/kg when administered on 4 consecutive days. During the daily administration, enzyme inhibition is seen in females after one day of treatment whereas cytochrome P-450 only becomes lowered after 4 days of administration. In males, no modification of this parameter is observed whereas the activities of microsomal monooxygenases are inhibited. These results suggest that N-nitrosocarbaryl could act on the active sites of the enzymes which metabolize aniline and p-nitroanisole.

Aniline Hydroxylase↗
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↗