[Hepatosplenic lesions due to a systemic bartonellosis in an immunocompetent patient]. / Atteinte hépato-splénique et bartonellose systémique chez une patiente immunocompétente.

We describe a case of a young healthy patient who presents a lot of hepato-splenic lesions caused by a systemic cat scratch disease. This case allows us to discuss the uncommon manifestations of the cat scratch disease and to describe the two types of hepatic lesions caused by a systemic bartonella infection : the granulomatosis and peliosis.

Nous rapportons le cas d'une jeune patiente immunocompétente présentant de multiples lésions hépato-spléniques secondaires à une infection systémique à bartonella. L'opportunité nous est ainsi donnée de discuter des manifestations rares de la maladie des griffes du chat ainsi que de décrire les deux types d'atteintes hépatiques causées par cette infection : la granulomatose et la péliose.

Chromosome-breaking activity of extracts of the mushroom Paxillus involutus Fries ex Batsch.

Dry and presoaked seeds of Nigella damascena were treated with aqueous extracts of the mushroom Paxillus involutus. At the first mitosis after the onset of germination, metaphase chromosomes showed damage independent of the origin of the mushrooms. The damaging substance(s) is (are) thermostable. Except a few achromatic gaps, all the lesions observed are of the chromosome type, i.e. are induced at the pre-synthetic G1 stage.

Induction of translocations in mouse spermatogonia after fractionated exposure to 60Co gamma-rays.

Male mice of the Q strain were exposed to 60Co gamma-rays at 2 Gy and 2 X 2 Gy separated by increasing time intervals (from 0 min to 4 min). The chromosome translocations induced in spermatogonia were scored at diakinesis-metaphase I. A significant decrease of the translocation frequency at time intervals higher than 2 min was observed, confirming results obtained with plant materials.

Low doses of pulsed ultrasound and chromosomal abnormalities in male mouse germ cells.

Male mice were exposed to pulsed ultrasound (intensity less than 1 mW, frequency 3.5 MHz) for 30 min or to sham treatment. After 30 h, 11, 12 or 13 days, the testes were cytologically and histologically examined (using squash preparations, air-drying and sections). The resulting damage was studied at diakinesis-metaphase I and II, spermatogonial metaphase and anaphase. The investigation by air-drying did not show any significant increase in chromosome damage, 30 h, 11, 12 and 13 days after treatment (spermatogonial and spermatocytic metaphases). There was, however, a significant increase of the frequency of aneuploid cells detected at metaphase II. Investigations by squash techniques or sections did not reveal adverse effects on the spindles at spermatogonial and spermatocytic anaphases. We suggest that the reduction of fertility previously observed in our clinic could be explained by an increase of aneuploidy if germ cells are exposed to ultrasound during diakinesis of the first meiotic division.

In vivo mutagenicity evaluation of domperidone in Drosophila germ cells and rat bone marrow cells.

Possible induction of chromosome aberrations and gene mutations by domperidone was studied in vivo respectively by a micronucleus test on female rats and a sex-linked recessive lethal test on Drosophila. In accordance with previous results all these studies revealed negative findings for domperidone so that it can be concluded that domperidone has no potential to induce chromosome aberrations and/or gene mutations.

Mutagenic efficiency of organophosphorus insecticides used in combined treatments.

Male mice (Q strain) received two consecutive injections of organophosphorus insecticides: a phosphonate (trichlorfon) was combined to a thiophosphate (methylparathion) or a dithiophosphate (malathion or methylazinphos) in order to evaluate the interactions at the genetic and cytogenetic levels. No increase in chromosome damage was observed in bone marrow cells, spermatogonia, and primary spermatocytes. In a dominant lethal mutation assay, the frequency of postimplantation lethality was not significantly increased over the control level. The percentage of preimplantation losses was enhanced, probably due to a toxic effect on male germ cells.

Cytogenetic and genetic effects of subchronic treatments with organophosphorus insecticides.

Male mice (Q strain) received 5 days a week for 7 weeks drinking water containing dichlorvos (2 ppm), dimethoate (0.6 ppm), malathion (8 ppm), methylparathion (0.15 ppm), or trichlorfon (0.5 ppm). At the end of the treatment, no chromosome damage was observed in bone marrow cells, spermatogonia, and primary spermatocytes. Dominant lethal mutation assays were performed to investigate the pre- and postimplantation foetal lethality. Only negative results were obtained.

Evaluation of the mutagenic potential of four commercial mixtures of insecticides.

Male mice (Q strain) were given a single ip injection at the maximum tolerated dose of one of four commercial mixtures of insecticides: Luxan Tue-Taons (150 g dimethoate and 150 g fenitrothion/litre), Metadipterex (210 g trichlorfon and 270 g methyldemeton/litre), Dynafos (155 g malathion, 60 g dichlorvos and 75 g carbaryl/litre) and Phosan Plus (95 g dimethoate, 100 g malathion and 100 g methoxychlor/litre). At the maximum tolerated doses, Luxan Tue-Taons (60 mg/kg), Metadipterex (15 mg/kg), Dynafos (50 mg/kg) and Phosan Plus (100 mg/kg) did not induce chromosome aberrations in bone-marrow cells, spermatogonia or primary spermatocytes of the mice. No evidence of potential genetic effects was obtained in a dominant lethal mutation assay.

Absence of genetic and cytogenetic effects in mice treated by the organophosphorus insecticide parathion, its methyl analogue, and paraoxon.

Male mice (Q strain) received a single i.p. injection of 3 organophosphorus compounds: ethylparathion (10 mg/kg), its methyl analogue (methylparathion, 10 mg/kg), or its phosphate derivative (ethylparaoxon, 0.3 mg/kg). The number of chromosome aberrations observed in bone marrow cells and spermatogonia, and the frequency of pre- and postimplantation foetal lethality obtained in a dominant lethal mutation assay, did not conclusively prove that the tested compounds produced a mutagenic effect.

Genetic and cytogenetic effects induced in the mouse by an organophosphorus insecticide: malathion.

Male mice (Q strain) received an ip injection of malathion (300 mg/kg). The percentage of chromosome aberrations was not increased in both bone marrow cells and spermatogonia. In a dominant lethal mutation assay, the frequency of pre- and postimplantation fetal lethality was not significantly enhanced over the control level.

Cytogenetic effects induced by organophosphorus pesticides in mouse spermatocytes.

Male mice (Q strain) received a single i.p. injection of 14 organophosphorus compounds, including 11 insecticides, administered on separate occasions. After a recovery period of 10 to 15 days, the cytogenic effects were analyzed in primary spermatocytes at diakinesis-metaphase I corresponding to the treatment of A4-B type spermatogonia. At the highest tolerated dose, trimethylphosphate (1000 mg/kg), triethylphosphate (300 mg/kg), dichlorvos (10 mg/kg), methylparathion (10 mg/kg), ethylparathion (10 mg/kg), ethylparaoxon (0.3 mg/kg), fenitrothion (1000 mg/kg), methylbromophos (1000 mg/kg), ethylbromophos (1000 mg/kg), dimethoate (10 mg/kg), malathion (300 mg/kg), methylazinphos (1 mg/kg), ethylazinphos (1 mg/kg) and trichlorfon (100 mg/kg) did not produce chromosome damage.

Genetic and cytogenetic effects of Fenitrothion.

Male mice (Q strain) were injected intraperitoneally with a high dose (i.e., 1 g/kg) of the organophosphorus insecticide Fenitrothion. No increase in the percentage of chromosome aberrations was observed in bone marrow cells and spermatogonia. A dominant lethal mutation assay did not show any enhancement of fetal mortality before or after implantation.

Mutagenicity of some organophosphorus compounds at the ade6 locus of Schizosaccharomyces pombe.

12 organophosphorus insecticides were tested for toxicity and mutagenicity in the forward mutation test system ade6 of the yeast Schizosaccharomyces pombe. EMS and MMS were selected as positive controls. 3 compounds, dichlorvos, trichlorfon and paraoxon, showed a linear dose-response relationship. Among the other compounds investigated, methyl derivatives, though in general more toxic than ethyl derivatives, did not significantly increase the mutation frequency. Trichlorfon, tested in combination with malathion, methylparathion or methylazinphos (guthion), produced clearly synergistic effects for both toxicity and mutagenicity. The addition of S9 microsomal liver fraction decreased the efficiency of both single and combined treatments only where a dose-response relationship or a synergistic effect was obtained.

Genotoxicity of an organophosphorus insecticide, dimethoate, in the mouse.

The effects of dimethoate were investigated in the mouse after acute (10 mg/kg i.p.) or chronic treatment (0.6 ppm, 5 days a week for 7 weeks). Dominant lethal mutations were scored for a 7-week period after the acute dose, and immediately after exposure for the chronic dose. Chromosome damage was also analysed in bone marrow and spermatogonial cells at the same dose levels (from 12 to 48 h after treatment). MMS (60 mg/kg i.p.) was chosen as the positive control. In no experiment did dimethoate show any genotoxicity.