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J Fränz

Publications and source records attributed to J Fränz.

15 recordsLinked to original sources

Induction of sister-chromatid exchanges by chemotherapeutic drugs in spermatogonia of mice: effects of procarbazine, adriamycin, cyclophosphamide and mitomycin C.

The chemotherapeutic drugs procarbazine (PCB), adriamycin (ADR), cyclophosphamide (CP) and mitomycin C (MMC) were evaluated in vivo for induction of sister-chromatid exchanges (SCEs) in differentiating spermatogonia of mice. There was a dose-dependent increase in SCE induced by the drugs. The lowest doses that enhanced the SCE rate to greater than twice baseline frequency were: 10 (PCB), 0.25 (ADR), 5 (CP) and 0.25 (MMC) mg/kg body weight. Based on the x-fold increase in SCE over baseline frequency, induced by the highest test dose (which permitted analysis of SCE), the drugs evaluated were ranked as follows: CP greater than MMC greater than PCB greater than ADR. The persistence of SCE-inducing lesions in spermatogonia was investigated by giving a treatment of CP (20 mg/kg body weight), 6 and 9 days before completion of 5-bromodeoxyuridine (BrdUrd) administration. Within 6-9 days, the SCE rate returned to the baseline level.

Animals

Chromosome analysis of bone marrow in mammals after treatment with isoniazid.

Cytogenetic investigations in bone marrow from animals treated with isoniazid (INH) were performed in seven different laboratories according to a standard protocol. The experiments were carried out in the Chinese hamster, the mouse, and the rat. In short-term studies INH was administered twice at an interval of 24 h in doses of 5, 25, and 125 mg/kg, and the animals were sacrificed 6, 12, 24, and 48 h after the second dose. In long-term studies doses of 25 and 125 mg/kg were administered thrice weekly for 12 weeks. As a rule, each group consisted of at least four animals, and 100 metaphases per animal were counted. Statistical analysis of the data showed that the incidence of chromosomal aberrations including gaps lay in the critical range for two groups in one laboratory and was significantly higher than in the control in three groups in another of the seven laboratories. From the results of both the short-term and the long-term studies in all laboratories, however, it may be concluded, that isoniazid does not induce gross chromosomal aberrations.

Animals

Mutagenicity of isoniazid: testing for somatic chromosome aberrations in mouse embryos.

Isonicotinic acid hydrazide (INH) were given by peroral intubation to pregnant mice of strain C57BL/6Ffm on day 9 of pregnancy, INH was given in the following doses: 0, 5, 25, and 125 mg/kg solved in physiological saline. Cytogenetic analysis of homogenized embryos 6, 12, 24, and 48 h, resp., after treatment of the females did not show any increase of the rate of gaps or chromosomal aberrations.

Animals

[Family studies for detection of latent psoriatics by assay of alterations in steroid metabolism (author's transl)].

In psoriasis changes of the DHEA metabolism could be demonstrated. These genetically determined basic alterations may represent an important factor for the manifestation of psoriasis. They consist of a decreased penetration of DHEA through the cell membrane and an increased reduction of DHEA to ADIOL, leading to a reduced DHEA/ADIOL ratio. In the present investigations the question was whether the assay of these parameters may aid in the detection of latent psoriasis. For this purpose 31 members form 6 unselected families of psoriatics (8 manifested psoriatics, 18 potential psoriatics, 5 clinically and anamnestically healthy family members by marriage) as well as 6 further controls were examined. It could be shown that those changes in the DHEA metabolism, which are evident in manifested psoriatics also occur at least in part of potential psoriatics. However, both parameters investigated do not always behave the same way. Hence, from the present data a satisfactory diagnosis of latent psoriasis does not seem possible. Still, the estimation of the above parameters may aid in the attempts to define latent psoriasis. Further investigations of such families are warranted for final elucidation of this problem.

Androstenediols