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Biomedical subjects

P M Conklin

Publications and source records attributed to P M Conklin.

6 recordsLinked to original sources
PubMed1986

Mutation and enhanced virus transformation of cultured hamster cells by exposure to gaseous ethylene oxide.

Ethylene oxide is a classical mutagen and a carcinogen based on evidence from studies in experimental animals. It is widely distributed in industrial, research, hospital, and food environments. In an effort to explore the use of newly developed methods for exposing mammalian cells to gaseous or volatile mutagens/carcinogens, Chinese hamster V79 cells were treated for 2 hr with gaseous ethylene oxide, in sealed treatment chambers, and assayed for survival and mutagenic response by analysis of induced resistance to 6-thioguanine or ouabain. Significant numbers of mutants were produced at both genetic markers by 1,250-7,500 ppm ethylene oxide. Similarly, primary Syrian hamster embryo cells were treated for 2 or 20 hr with gaseous ethylene oxide in sealed treatment chambers and subsequently assayed for survival and increased sensitivity to SA7 virus transformation. Treatment concentrations extended from toxic to several nontoxic concentrations. After 2-hr ethylene oxide treatment at 625-2,500 ppm a significant enhancement of virus transformation was observed. At 20 hr after treatment no enhancement was observed. Treatment of hamster cells with ethylene oxide in both bioassay systems yielded concentration-related, quantitative results.

Adenoviruses, Simian↗
PubMed1983

Synergism in the transformation of hamster embryo cells treated with formaldehyde and adenovirus.

Formaldehyde is a large production volume chemical widely distributed in research laboratories, industrial workplaces, and home and personal environments. Inhalation studies with formaldehyde have documented its ability to produce squamous cell carcinomas in rats. When primary hamster embryo cells were treated by gaseous exposure to formaldehyde or by incorporation into the medium, a dose-related increase in the frequency of SA7 virus transformation was produced. The length of chemical treatment and the time interval before subsequent addition of transforming virus was critical, with two-hr treatment times as the most efficient. Treatment by gaseous exposure permitted utilization of lower treatment concentrations. Determination of formaldehyde concentrations in culture media of bioassay dishes treated by this method documented that 2.2 micrograms/ml produced significantly enhanced viral transformation. Exposure of hamster embryo cells to formaldehyde by these methods produces reproducible and quantitative genotoxic effects.

Adenoviridae↗
PubMed1975

Body surface area in the infant rat.

Body surface area (SA), one index used to minimize size differences in metabolic studies, was estimated by a coating method in rats aged 1, 7, 14, and 21 days (d) (n = 100-107). Body weights (BW) at each age varied about twofold. Regression equations were calculated for SA (cm2) vs. BW (g) (SA = 8.73 + 2.29 BW, 17.79 + 1.71 BW, -4.92 + 2.16 BW, and 53.68 + .82 BW at 1, 7, 14, and 21 days, respectively) and log SA vs. log BW (SA = 6.71 BW0-667, 9.12 BW0-577, 1.73 BW1-042, and 18.97 BW0-412). All the latter differed significantly from SA = 10 BE2/3, frequently used with adult mammals. Correlation coefficients were approximately 0.6-0.9 and did not differ with mode of expressing results. Regressions, whether linear or logarithmic, differed significantly among ages, apparently reflecting appreciable conformational changes in the rapidly growing and maturing preweanling rat.

Age Factors↗
PubMedDate not supplied

Mutagenesis of xeroderma pigmentosum fibroblasts by acrolein.

Acrolein, a short-chain aldehyde encountered as a component of tobacco smoke and as a ubiquitous environmental contaminant, was tested for its toxic and mutagenic effects toward human fibroblast cells. We found that human cells characterized by a deficiency in DNA repair (cells from xeroderma pigmentosum (XP) patients) were much more sensitive (D37 approximately equal to 0.25 microM) to the cytotoxic effects of acrolein than were cells from normal individuals (D37 approximately equal to 0.8 microM). Acrolein was also strongly mutagenic to the XP cells (a dose response was observed between 0.2 and 0.8 microM acrolein); however acrolein did not induce an increase in the mutant frequency of normal fibroblasts. Possible reasons for this apparent lack of mutagenicity in normal human cells are discussed.

Acrolein↗