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Biomedical subjects

D L Putman

Publications and source records attributed to D L Putman.

28 records · Page 2Linked to original sources
PubMed1985

Dose-responsive increase in sister-chromatid exchanges in bone-marrow cells of mice exposed nose-only to whole cigarette smoke.

The effect of whole cigarette smoke exposure on bone-marrow sister-chromatid exchanges (SCEs) was studied in B6C3F1 mice. Animals were exposed nose-only to 10% (v/v) cigarette smoke 5 days/week for 2 weeks. Four dose levels of cigarette smoke (1, 4, 9 and 18 exposures/day) were studied using 2 cigarette types, Kentucky reference 3A1 (3A1) and American Blend (AB). A single exposure represented approximately 1 cigarette. A dose-dependent increase in SCEs was observed for both the 3A1 and AB cigarettes at dose levels which had no effect on bone-marrow cell-replication kinetics. These findings represent the first demonstration of a dose-responsive increase in cigarette smoke-induced SCEs in a rodent model system.

Animals↗
PubMed1984

Effect of 3-aminobenzamide on the induction of toxicity and transformation by ethyl methanesulfonate and methylcholanthrene in BALB/3T3 cells.

3-Aminobenzamide, a potent inhibitor of nuclear poly ADP-ribosyl synthetase, was tested for its ability to alter the toxic and/or transforming effects of ethyl methanesulfonate, methyl methanesulfonate and 3-methylcholanthrene in BALB/3T3 clone A31-1 cells. 3-Aminobenzamide enhanced the toxic effects of both ethyl methanesulfonate and methyl methanesulfonate in a dose dependent manner, but had minimal effects on 3-methylcholanthrene induced toxicity. Similarly, 3-aminobenzamide greatly enhanced ethyl methanesulfonate induced transformation while failing to enhance the transformation of BALB/3T3 clone A31-1 cells by 3-methylcholanthrene. These results stress the importance of poly ADP-ribosyl synthetase in repair of DNA damage and the chemical induction of transformation in vitro.

Animals↗
PubMed1983

Cytogenetic evaluation of di-(2-ethylhexyl)phthalate and its major metabolites in Fischer 344 rats.

Di-(2-ethylhexyl)phthalate (DEHP) and its two major metabolites, mono-(2-ethylhexyl)phthalate (MEHP) and 2-ethylhexanol (EH), were evaluated for their ability to induce chromosomal damage in male Fischer 344 rats after oral administration. Dose levels, the highest of which represents one-tenth of the five-day LD50, were based on a preliminary five-day dose-finding study for each test material. The dose levels selected were 5.0, 1.7, and 0.5 ml/kg/day for DEHP; 0.14, 0.05 and 0.01 ml/kg/day for MEHP; and 0.21, 0.07 and 0.02 ml/kg/day for EH. All test materials and vehicle control (corn oil) were administered by gavage for five consecutive days. A triethylenemelamine (TEM)-positive control group received a single intraperitoneal injection of 0.5 mg/kg TEM one day prior to sacrifice. Of the 50 metaphase bone marrow cells examined from each animal, no significant increase in chromatid and chromosome breaks or structural rearrangements were noted for DEHP, MEHP, and EH. In addition, the mitotic index, determined from 100 cells per animal, was unaffected by DEHP, MEHP, or EH. The results of this investigation indicate that DEHP, MEHP, and EH, at these dose levels, did not induce detectable chromosomal aberrations after oral administration.

Animals↗
PubMed1983

Genetics of xenotropic virus expression in mice. II. Expression of major virus structural proteins in crosses involving NZB/B1NJ, SWR/J, and 129/J strains of mice.

The expression of viral structural polypeptides and the production of infectious xenotropic virus were found to segregate together in NZB, 129/J, and SWR/J mice and in crosses between these strains. The viral p30 protein segregation pattern, as measured by competition radioimmunoassay using extracts of frozen spleens from backcross progeny, indicate that xenotropic murine leukemia virus expression is controlled by two dominant genes.

Animals↗
PubMed1978

Adoptive immunochemotherapy of a transplantable AKR leukemia (K36).

Adoptive immunotherapy of a transplantable AKR leukemia (K36) was carried out as an adjunct to cytoxan chemotherapy using normal allogeneic H-2-incompatible spleen cells as well as sensitized H-2-matched allogeneic spleen cells. A significant therapeutic effect was obtained with cytoxan and allogeneic C57BL/6 splenocytes, demonstrating the potential use of the graft-versus-host reaction. Utilizing specific adoptive immunochemotherapy, a maximum effect was found with splenocytes from allogeneic but H-2-compatible CBA/J mice immunized against an allogeneic Gross-virus-induced lymphoma (E female G2). This therapeutic effect was most likely the result of prior sensitization of donor lymphocytes to common virus-associated tumor antigens.

Animals↗
PubMed1977

Characterization of human cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine.

Human osteosarcoma (HOS) clonal cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were characterized, and compared to non-producer HOS cells transformed by Kirsten murine sarcoma virus (Ki-MSV). The MNNG- and virus-transformed cells grew in the aggregate form above an agar base, grew in soft agar, and had a high fibrinolytic activity. When inoculated into nude mice, all the chemically or virally altered cells produced tumors or tumor nodules. When transplanted into ATS-treated hamsters, the cells transformed by MNNG (0.01 mug/ml) and Ki-MSV produced tumors but MNNG (0.1 mug/ml) transformed cells did not produce tumors. The control HOS cells did not grow in the aggregate form but formed colonies in soft agar, and had low fibrinolytic activity and no capacity to form tumors in nude mice and ATS-treated hamsters. However, one of the control clonal lines had a high level of fibrinolytic activity. Cellular aggregation properties of human transformed cells did appear to correlate with tumorigenicity in nude mice.

Animals↗
PubMedDate not supplied

Evaluation of the genotoxic potential of zinc pyrithione in the Salmonella mutagenicity (Ames) assay, CHO/HGPRT gene mutation assay and mouse micronucleus assay.

The mutagenic potential of zinc pyrithione (Znpt) was evaluated in vitro in the Salmonella/mammalian microsome plate incorporation mutagenicity (Ames) assay and the CHO/HGPRT gene mutation assay. The clastogenic potential of Znpt was evaluated in vivo using the mouse micronucleus test. Znpt was negative in the Ames test in five tester strains in the presence and absence of rat liver microsomal enzymes when assayed at concentrations ranging between 10 and 333 micrograms per plate and between 0.03 and 33 micrograms per plate, respectively. Znpt also produced negative results in the CHO/HGPRT assay. No significant increases in mutant frequencies were seen in the presence and absence of rat liver microsomal enzymes. In each case, the highest concentrations reduced cellular viability by 83% and 85%, respectively. Znpt also did not induce increased frequencies of micronuclei in mouse bone marrow cells when tested at the maximally tolerated dose (MTD) (44 mg kg-1). These data support the conclusion that Znpt lacks genotoxic activity under the conditions of these tests.

Animals↗
PubMedDate not supplied

Cytogenetic studies on commercial hexane solvent.

Commercial hexane is a solvent mixture of six-carbon isomers, consisting principally of n-hexane, 3-methylpentane, methylcyclopentane and 2-methylpentane. The potential of commercial hexane to produce chromosome aberrations was evaluated in both an in vitro assay using Chinese hamster ovary (CHO) cells and an in vivo cytogenetics assay using Sprague-Dawley rats. The CHO cells were exposed to media containing commercial hexane at concentrations of 0.014-0.42 microliters ml-1 in the presence and absence of an S-9 activation mixture. Cellular toxicity was observed at the higher dose levels, but no increase in chromosome aberrations was observed in either the non-activated or S-9-activated systems. For the in vivo cytogenetics assay, rats were exposed nose-only for 6 h per day for 5 consecutive days to commercial hexane vapor at target concentrations of 900, 3000 and 9000 ppm. Bone marrow cells were collected at 6 and 24 h after the midpoint of the last exposure. Metaphase cells were examined microscopically for chromosome aberrations. No statistically significant increases in aberrant cells were observed in the commercial hexane-exposed animals of any dose group at either of the bone marrow harvest times. In conclusion, commercial hexane did not produce chromosomal mutations under the conditions of these studies.

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