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Biomedical subjects

D F Callen

Publications and source records attributed to D F Callen.

189 records · Page 11Linked to original sources
PubMed1977

Comparison of the genetic activity of aflatoxins B1 and G1 in Escherichia coli and Saccharomyces cerevisiae.

The ability of aflatoxins B1 and G1 to induce back mutations to arg+ in Escherichia coli K-12/343/113 was compared with the induction of mitotic gene conversion to ade+ in the diploid yeast strain Saccharomyces cerevisiae D4, ade-2. In analogy to previous results with other microorganisms, the compounds were not genetically active per se, indicating that under the experimental conditions employed none of the tester strains were able to activate the compounds to mutagenic products. In experiments using liver homogenates (S-9 fraction) of male Golden Syrian hamsters previously treated with phenobarbital, aflatoxin B1 exhibited strong genetic activity both in E. coli and in S. cerevisiae, whereas the mutagenic activity of aflatoxin G1 was markedly lower and could be detected only in the E. coli tester strain. These results correlate the findings that aflatoxin G1 is a less potent carcinogen and mutagen than aflatoxin B1.

Aflatoxins↗
PubMed1977

Mutation induction by the antischistosomal drug F30066 in various test systems.

The genetic activity of furapromidium (F30066), an antischistosomal drug, was studied in Salmonella typhimurium, Saccharomyces cerevisiae, Neurospora crassa and cultured Chinese hamster cells. The results show that F30066 induces gene mutations in S. typhimurium, N. crassa and Chinese hamster cells. This compound also causes gene conversions in S. cerevisiae.

Acrylamides↗
PubMedDate not supplied

Mapping of a new RFLP marker RN1 (DXS369) close to the fragile site FRAXA on Xq27-q28.

A new polymorphic DNA marker RN1, defining locus DXS369, was recently isolated. Using different somatic cell hybrids, RN1 was mapped between markers 4D-8 and U6.2. We have narrowed the localization of RN1 to the region between 4D-8 and FRAXA by genetic mapping in fragile X [fra(X)] families. Combined with information from other reports, the following order of loci on Xq27-q28 is suggested: cen-F9-(DXS105-DXS152)-DXS98-DXS369-FRAXA- DXS304-(DXS52-DXS15-F8)-tel. The locus DXS369 is closely linked to FRAXA, with a peak lodscore of 18.5 at a recombination fraction of 0.05. Therefore, RN1 is a useful probe for carrier detection and prenatal diagnosis in fra(X) families.

Animals↗
PubMedDate not supplied

Genomic structure and expression analysis of the spastic paraplegia gene, SPG7.

SPG7 is a newly identified gene involved in an autosomal recessive form of hereditary spastic paraplegia (HSP), a genetically heterogeneous group of neurodegenerative disorders. This gene encodes a protein characterized as a nuclear-encoded mitochondrial metalloprotease. The present report describes the genomic structure of the SPG7 gene. It is organized into 17 exons ranging from 78 to 242 bp and spans approximately 52 kb within three overlapping cosmids. The exon/intron boundaries and all splice junctions are consistent with the published consensus sequences for donor and acceptor sites. The provided genomic structure of SPG7 should facilitate the screening for mutations in this gene in patients with HSP and other related mitochondrial disease syndromes. SPG7 has been mapped to chromosome 16q24.3, a region of frequent loss of heterozygosity (LOH) seen in sporadic breast and prostate cancer. We have performed single-strand conformation polymorphism analysis of ten exons of this gene in a number of sporadic breast cancer samples showing LOH at 16q24.3. No mutations were detected; only single nucleotide polymorphisms were observed in exon 11, intron 7, intron 10 and intron 12. An expression analysis study has revealed the differential expression of SPG7 mRNA in various tissues and at different developmental stages.

ATPases Associated with Diverse Cellular Activitie↗
PubMedDate not supplied

Toxic and genetic effects of fuel oil photoproducts and three hydroperoxides in Saccharomyces cerevisiae.

Phototransformation of no. 2 fuel oil by UV irradiation at wavelengths designed to simulate sunlight resulted in the formation of products toxic to the yeast Saccharomyces cerevisiae. Increasing the time of irradiation of the fuel oil samples increased the toxicity. Fuel oil that had been irradiated for 12 or 24 h was convertagenic to the yeast strain D4. The toxicity and genetic activity of these samples could be removed by treatment with thiacyclohexane. It is thought that hydroperoxides are the primary photoproducts responsible for these biological effects. Of three hydroperoxides tested, tert-butyl was convertagenic and cumene and tetralin were not. However, all three hydroperoxides were toxic to yeast.

Fuel Oils↗
PubMedDate not supplied

Comparison of the genetic activity of 5-nitroimidazole derivatives in Escherichia coli, Neurospora crassa, Saccharomyces cerevisiae and Drosophila melanogaster.

5-nitroimidazoles, including metronidazole (compound 1) and 3 analogues (compounds 2, 3 and 4) of actual or potential chemotherapeutic use were assayed for genetic activity in test systems detecting forward and back mutations in Escherichia coli K-12/343/113, forward mutations in Neurospora crassa heterokaryon 12, mitotic gene conversion in the heteroallelic diploid yeast strain Saccharomyces cerevisiae D4 and sex-linked recessive lethals in Drosophila melanogaster. Whereas metronidazole exhibits moderate mutagenic activity in E. coli, two of the analogues, compounds 2 and 3 are strongly mutagenic even at concentrations that do not inactive the colony forming ability of the cells. The analogue compound 4 does not show any effect toward E. coli under the present experimental conditions. Similar results were obtained with N. crassa, with S. cerevisiae and with Drosophila in which compound 2 exhibits the highest effect, while compound 4 is non-mutagenic in all assays. These biological effects have been partly explained on the basis of differences in the chemical structure of the compounds.

Animals↗