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Biomedical subjects

D Anderson

Publications and source records attributed to D Anderson.

At least 505 records · Page 28Linked to original sources
PubMed1986

Studies on the genetic effects of phthalic acid esters on cells in culture.

Mono(2-ethylhexyl) phthalate (MEHP) induced chromosome aberrations in cells of two culture lines, one derived from Chinese hamster ovary cells (CHO) and the other from rat liver cells (RL4). In CHO cells, the clastogenicity of MEHP was unaffected by the presence of an exogenous metabolic activation system (S-9 mix). 2-Ethylhexanol, o-phthalic acid, and phthalic anhydride were without effect. Cytochemical methods and assays for carnitine acetyltransferase and KCN-insensitive palmitoyl CoA oxidation were employed to determine whether chromosome damage was associated with peroxisome proliferation. No evidence of an increase in peroxisome numbers or of induction of marker enzymes was found in CHO cells treated with MEHP for up to 72 hr. Clofibric acid and BR931 were also ineffective. Observations on changes in CHO cell structure and permeability, and on the haemolytic effects of phthalate monoesters, suggest that the cytotoxicity of MEHP may be due primarily to its action on cell membranes. Since chromosome damage was observed only at cytotoxic concentrations, it is suggested that damage to lysosomal membranes and the release of endonucleases may be responsible for the observed clastogenicity of MEHP in vitro.

Animals↗
PubMed1985

Infectious and bleeding complications in patients with glycogenosis Ib.

Clinical, hematologic, and immunologic findings were reviewed in 21 patients with glycogenosis Ib. Fifteen of the patients suffered from moderate to severe bacterial infections. Ten patients had excessive epistaxis or bleeding from surgical sites, and eight suffered oral and anal mucosal ulceration. Sixteen of 21 patients exhibited chronic neutropenia associated with abnormalities in myeloid maturation and decreases in the bone marrow storage and peripheral marginating pools. Diminished neutrophil motility was documented in 14 of 15 patients tested, and adherence was decreased in three patients studied. Neutrophil microbicidal activity, reduction of nitroblue tetrazolium, and ingestion were normal in all patients tested. Bleeding times were prolonged in five of eight patients, and results of platelet function studies were abnormal in five individuals. Excessive bleeding in patients with glycogenoses Ia and Ib are similar and may be secondary to the functional deficiency of glucose-6-phosphatase. However, neutropenia, neutrophil dysfunction, and the resulting infectious complications are specific for Ib disease and may be related to abnormal glucose-6-phosphate transport.

Adolescent↗
PubMed1985

Left ear suppression on verbal dichotic tests in patients with multiple sclerosis.

Verbal dichotic listening tests employing nonsense consonant-vowel stimulus pairs were administered to 11 right-handed patients with chronic multiple sclerosis and to 10 right-handed normal controls. A highly significant reduction of left-ear scores was found in the multiple sclerosis group. We propose that the basis for this finding is a disconnection of the auditory callosal pathway and that dichotic listening tests may be of value in detecting the presence of lesions of the deep white matter of the cerebral hemispheres in multiple sclerosis.

Adult↗
PubMed1985

Induction of mutation and chromosome damage by excess bases and nucleosides.

The studies reported in this communication were conducted to determine if naturally occurring cell constituents could themselves cause mutation. All the bases and their corresponding nucleosides have been shown in culture to produce chromosome damage in P388 mouse lymphoma and Chinese hamster ovary cells (CHO) and adenosine has produced an increased incidence of sister chromatid exchanges in CHO cells. In addition thymidine has produced an increase in V79 cells resistant to 8-azaguanine and ouabain, although no effects were seen in six strains of Salmonella typhimurium. Such damage probably arises as a result of imbalanced DNA-precursor pools. Thus mutagenic events may arise by mechanisms unrelated to direct alterations of DNA.

Adenosine↗
PubMed1985

Nitrofurazone--genotoxicity studies in mammalian cells in vitro and in vivo.

Nitrofurazone has been examined for genetic effects in mammalian cells in vitro and in vivo. In the in vitro studies in Chinese hamster ovary (CHO) cells, metaphase analysis was carried out at different sampling times after nitrofurazone treatment and gene mutation leading to hypoxanthine-guanine phosphoribosyltransferase deficiency was also investigated. Both assays were carried out in the presence and absence of a metabolic activation system (S-9 mix). Metaphase analysis was also carried out on bone-marrow cells at various sampling times after treatment of rats with a single oral dose of nitrofurazone and at one sampling time after administration of five daily oral doses. In the in vitro studies a dose-related increase in aberrant metaphases was observed after nitrofurazone treatment both with and without metabolic activation, but the gene mutation assay was negative. In vivo, despite the use of high doses of nitrofurazone (up to 400 mg/kg body weight) resulting in evidence of toxicity and a reduction in the mitotic index of bone-marrow cells, there was no evidence that nitrofurazone increased chromosomal damage. It is concluded that although the compound has the capacity to cause chromosomal damage in mammalian cells in vitro, it is detoxified by the metabolic system of the animal. These results, together with existing in vivo data, do not suggest that nitrofurazone is likely to give rise to any genotoxic hazard for man.

Animals↗
PubMed1985

Genetic toxicology in the food industry.

In vitro testing of food products for mutagenic activity presents particular problems, especially in connection with the administration of the test material to the assay system, the possible interference of food components with the genetic end-point used for the assay, the presence in foods of various factors that may modify mutagenic activity, the identification of appropriate negative or positive controls and the avoidance of artefactual mutagen formation during the preparation of test samples. Ideally mutagenicity testing requires in vivo studies (although these too have particular problems when applied to foods) but, at present, in vitro tests provide the only practical means of screening large numbers of food samples or modifying factors and of assessing food-processing techniques. The tests can be carried out on model systems (e.g. amino acid/sugar mixtures), on isolated and purified constituents of foods, on fractionated solvent extracts or on whole-food homogenates subjected to digestion procedures. However, to determine genotoxic risk from foodstuffs, quantitative data from mammalian in vivo tests and from human consumption and metabolism studies are also required.

Animals↗
PubMed1985

Suitability of the P388F mouse lymphoma system for detecting potential carcinogens and mutagens.

The P388F mouse lymphoma (TK +/-) system has been evaluated further for use as a primary mammalian-cell test and as a complementary assay to the Ames Salmonella reverse-mutation assay. The system showed a clear dose response with three alkylating agents of previously demonstrated genotoxic potential and gave the anticipated positive result with benzo[a]pyrene in the presence of S-9 mix. In addition, while giving the expected negative result with sugar, the assay detected genotoxic activity in hexamethylphosphoramide, acrylonitrile and formaldehyde, all of which are known to give negative results in the Ames test.

Animals↗
PubMed1985

The mutagenic properties of N-nitrosopeptides in the Ames test.

N-(N-Acetyl-L-prolyl)-N-nitrosoglycine (APNG) and N-(N-acetylvalyl)-N-nitrosoglycine (AVNG) are shown to exert mutagenic activity in the Salmonella/mammalian microsome mutagenicity (Ames) test. Positive responses are apparent for base-pair substitution mutation-detecting strains (TA1535, TA100 and TA102) both with and without the addition of S9-mix. It is concluded that both APNG and AVNG are direct-acting mutagens.

Animals↗