Biomedical subjects

Adolf Baumgartner

Publications and source records attributed to Adolf Baumgartner.

4 recordsLinked to original sources

PubMed2006

Chromosome-specific DNA repeat probes.

In research as well as in clinical applications, fluorescence in situ hybridization (FISH) has gained increasing popularity as a highly sensitive technique to study cytogenetic changes. Today, hundreds of commercially available DNA probes serve the basic needs of the biomedical research community. Widespread applications, however, are often limited by the lack of appropriately labeled, specific nucleic acid probes. We describe two approaches for an expeditious preparation of chromosome-specific DNAs and the subsequent probe labeling with reporter molecules of choice. The described techniques allow the preparation of highly specific DNA repeat probes suitable for enumeration of chromosomes in interphase cell nuclei or tissue sections. In addition, there is no need for chromosome enrichment by flow cytometry and sorting or molecular cloning. Our PCR-based method uses either bacterial artificial chromosomes or human genomic DNA as templates with alpha-satellite-specific primers. Here we demonstrate the production of fluorochrome-labeled DNA repeat probes specific for human chromosomes 17 and 18 in just a few days without the need for highly specialized equipment and without the limitation to only a few fluorochrome labels.

Chromosomes, Artificial, Bacterial↗

PubMed2005

Time-course of radiation-induced chromosomal aberrations in tumor patients after radiotherapy.

PURPOSE: Radiation-induced chromosome aberrations are routinely used in biologic dosimetry to monitor radiation exposure. Translocations are considered stable aberrations with time after exposure. This study was performed to determine the temporal persistence of radiation-induced translocations during a 36-month period in therapeutically irradiated testicular seminoma patients who underwent partial body exposure (>10% of bone marrow). METHODS AND MATERIALS: Chromosome analyses were carried out in peripheral lymphocytes of 11 patients with testicular seminoma (n = 9), germinoma (n = 1), or follicular non-Hodgkin's lymphoma (n = 1). All patients received radiotherapy with photons from a linear accelerator; in 1 case, additional electron beams were used. Doses ranged from 26 Gy (seminoma) to 45 Gy (non-Hodgkin's lymphoma). None of the patients received chemotherapy. From each patient, blood samples were taken during the 36 months after irradiation at defined points. Chromosomal aberrations were scored after fluorescence in situ hybridization painting of chromosomes 1, 4, and 12 in combination with a pancentromeric probe. RESULTS: For 9 patients (7 with testicular seminoma, 1 with germinoma, and 1 with non-Hodgkin's lymphoma), a significant temporal decline of translocations, with a mean decline rate of 4.4% +/- 0.4% monthly, could be detected. Two testicular seminoma patients showed no temporal decline of aberration frequencies. CONCLUSION: Most partial body irradiated patients (9 of 11) showed a significant temporal decline of translocation frequencies during a 36-month period. Thus, reciprocal translocations after partial body irradiation cannot be regarded as stable over time. The temporal decline of aberration frequencies has to be taken into account for retrospective dose estimations.

Adult↗

PubMed2004

Antioxidants modulate thyroid hormone- and noradrenaline-induced DNA damage in human sperm.

The genotoxic effects of steroidal oestrogens are probably brought about by metabolic changes in their phenolic groups accompanied by the generation of quinones and reactive oxygen species. Although non-steroidal oestrogens and related compounds have not been thoroughly investigated for genotoxicity, some of them also contain phenolic groups that could be involved in redox cycling. Therefore, the aim of the present study was to evaluate the possible DNA-damaging effects of the thyroid hormones triiodothyronine (T3) and L-thyroxine sodium salt (T4) and the neurotransmitter noradrenaline (NA) in human sperm using the Comet assay. They were compared with diethylstilboestrol (DES), a steroidal oestrogen, as a positive control. After dose-response studies, doses of 80 microM T3, 80 microM T4, 300 microM NA and 175 microM DES, which produced DNA damage but retained good cell viability, were chosen for further experiments with the antioxidant catalase and the flavonoids kaempferol and quercetin. Since the scavenging enzyme catalase reduced the DNA-damaging effects of T3, T4 and NA, it can be surmised that these compounds under these conditions induced DNA damage mainly via the production of reactive oxygen species. This was further confirmed by the inhibitory responses produced by the flavonoids, which are known to have antioxidant effects. Therefore, the mechanism of mutagenic action of both steroidal and non-steroidal compounds imply the creation of oxidative stress and subsequent DNA damage due to reactive oxygen species and possibly due to reactive hormone derivatives created during their redox cycling.

Adult↗

PubMed2003

Oestrogenic compounds and oxidative stress (in human sperm and lymphocytes in the Comet assay).

Reactive oxygen species (ROS) are produced by a wide variety of chemicals and physiological processes in which enzymes catalyse the transfer of electrons from a substrate to molecular oxygen. The immediate products of such reactions, superoxide anion radicals and hydrogen peroxide can be metabolised by enzymes such as superoxide dismutase (SOD) and catalase (CAT), respectively, and depending on its concentration by Vitamin C (Vit C). Under certain circumstances the ROS form highly reactive hydroxyl radicals. We examined human sperm and lymphocytes after treatment with six oestrogenic compounds in the Comet assay, which measures DNA damage, and observed that all caused damage in both cell types. The damage was diminished in nearly all cases by catalase, and in some instances by SOD and Vit C. This response pattern was also seen with hydrogen peroxide. This similarity suggests that the oestrogen-mediated effects could be acting via the production of hydrogen peroxide since catalase always markedly reduced the response. The variable responses with SOD indicate a lesser involvement of superoxide anion radicals due to SOD-mediated conversion of superoxide to hydrogen peroxide generally causing a lower level of DNA damage than other ROS. The variable Vit C responses are explained by a reduction of hydrogen peroxide at low Vit C concentrations and a pro-oxidant activity at higher concentrations. Together these data provide evidence that inappropriate exposure to oestrogenic compounds could lead to free-radical mediated damage. It is believed that the observed activities were not generated by cell free cell culture conditions because increased responses were observed over and above control values when the compounds were added, and also increasing dose-response relationships have been found after treatment with such oestrogenic compounds in previously reported studies.

Adult↗