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Biomedical subjects

R E Kouri

Publications and source records attributed to R E Kouri.

At least 55 records · Page 3Linked to original sources
PubMed1979

Genetics of xenotropic virus expression in mice. I. Evidence for a single locus regulating spontaneous production of infectious virus in crosses involving NZB/B1NJ and 129/J strains of mice.

The extent of infectious xenotropic virus expression in homogenized splenic tissues from the high-virus-expressing NZB/BINJ mice and the non-virus-expressing 129/J mice and their crosses has been examined. The data suggest that a single autosomal "dominant-like" gene controls the spontaneous production and release of infectious xenotropic virus in NZB mice. Analysis of infectious virus production in second-backcross families [(F1 X 129) X 129] confirmed this conclusion. Variations in the amount of X-tropic virus released were evident in all genetic crosses. Virus titers (expressed as focus-forming units per milliliter) of supernatant fluid ranged from high levels in the NZB mice to somewhat lower levels in crosses involving the 129 mice. In the absence of a definite pattern in the titers observed in the genetic crosses studied, the term dominant-like is proposed for the single gene regulating the expression of X-tropic virus in NZB mice.

Animals↗
PubMed1979

Biological activity of tobacco smoke and tobacco smoke-related chemicals.

Exposure to whole cigarette smoke from reference cigarettes results in the prompt (peak activity is 6 hrs), but fairly weak (similar to 2 fold), induction of murine pulmonary microsomal monooxygenase activity. This activity can be detected by using as substrates either benzo(a)pyrene or ethoxyresorufin, and can be inhibited by treatment with cycloheximide or actinomycin D. Unlike the induction of pulmonary monooxygenases following intratracheal administration of 3-methylcholanthrene, these cigarette smoke-induced increases were not unequivocally linked to the Ah locus. Whole smoke condensate and fractions derived from these condensates can; a) induce pulmonary monooxygenase activity, b) inhibit benzo(a)pyrene metabolism in vitro, c) be metabolized to forms mutagenic to Salmonella typhimurium tester strains TA153, or TA98, d) transform C3H 10T1/2 cells in vitro, and e) enhance the carcinogenicity of benzo(a)pyrene in murine pulmonary tissue. A potentially important observation is that whereas hepatic tissue is capable of activating whole cigarette smoke condensate to mutagenic forms in vitro, murine pulmonary tissue does not seem capable of such activation. Although these pulmonary-derived tissue homogenates have significant AHH activity and can metabolize Aflatoxin B1, 2-aminofluorene and 7, 8-dihydro-7,8-dihydroxybenzo(a)pyrene to mutagenic forms, these homogenates fail to activate both cigarette smoke condensate and the pro-mutagen, 6-aminochrysene. These results are discussed with reference to the concept that whole cigarette smoke may be both a potential "initiator" and "promotor" of lung cancer in mice, and that this latter property may be the most important in determining cancer risk.

Animals↗
PubMed1978

Nucleoside phosphorylase 2 (Np-2) of mice.

Isozyme patterns of nucleoside phosphorylase (NP) in 16 inbred strains, two recombinant inbred, one congenic, and three species of wild mice were studied. Evidence is provided for a genetic locus, Np-2, encoding an electrophoretic variant which is expressed exclusively in erythrocytes of certain inbred strains. This finding establishes the occurrence of genetic polymorphism of NP among inbred strains of mice. In addition, the Npla allele previously reported only in inbred strains has been observed in one of the species of wild mice (Mus musculus castaneus) studied.

Animals↗
PubMed1977

3-methylcholanthrene-induced monooxygenase (O-deethylation) activity of human lymphocytes.

With a direct fluorescence assay, the levels of mixed-function oxidase activity were determined in mitogen-activated human lymphocytes. The O-deethylation of ethoxyresorufin to resorufin was used to quantitate mixed-function oxidase activity. Ethoxyresorufin O-deethylase activity was low to nondetectable in noninduced, mitogen-activated cells, but it was readily detected in 3-methylcholanthrene, mitogen-activated lymphocytes. The activity was: (a) dependent on assay time and number of lymphocytes; (b) dependent on the presence of reduced nicotinamide adenine dinucleotide phosphate; (c) stable to freezing at -80 degrees for at least 2 weeks; (d) reproducibly detected in duplicate samples of blood from one individual when cultured and assayed at the same time; but (e) quite variable in samples of blood from one individual at different times. Since in hepatic and pulmonary tissue of model animal systems ethoxyresorufin is a specific substrate for cytochrome P-448-associated monooxygenases, the use of this chemical could proffer an assay that specifically measures human cytochrome P-448-associated activity.

Adult↗
PubMed1976

Studies on pulmonary aryl hydrocarbon hydroxylase activity in inbred strains of mice.

Pulmonary and hepatic levels of aryl hydrocarbon hydroxylase (AHH) were studied in inbred strains of mice following intratracheal (i.t.) instillation of 3-methylcholanthrene (MCA). I.t. instillation of 188 mug MCA in sterile 0.2% gelatin in saline resulted in preferential induction of pulmonary AHH. After treatment with this dose of MCA, the pulmonary AHH levels of strains C57BL/6Cum, C57BL/6J, BALB/cMai, C3H/fMai, and C57L/J were observed to be induced within 24 h after treatment. Strains DBA/2Cum, AKR/J, SJL/J, DBA/2J and RF/J expressed no such increase. At a dose of 500 mug MCA, the pulmonary tissue of DBA/2 mice did express a 4-fold increase. This increase in AHH was determined to be quite different from the increase observed in C57BL/6 mice by: (1) specific activity of the enzymes, (2) genetic regulation, (3) susceptibility to inhibition by 7,8-benzoflavone, and (4) spectral properties of the associated cytochromes. It was of major importance that induction of pulmonary AHH was observed to be regulated by a single dominant gene in crosses involving the C57BL/6Cum and DBA/2Cum strains of mice. Results were discussed with the view in mind that these genetically regulated levels of AHH may play a role in susceptibility to cancers induced by polycyclic aromatic hydrocarbon carcinogens.

Animals↗
PubMed1975

Correlation between balance of specific chromosomes and expression of malignancy in hamster cells.

Four 1-theta-D-arabinofuranosylcytosine (ara-C)-and one dimethylnitrosamine-transformed Syrian hamster cell lines were established. All produced tumors when inoculated into newborn hamsters. Specific chromosome changes were found in these lines consistent with changes observed recently by other investigators. Clones that had either high or low malignant potential were derived from two fibrosarcomas produced by one of the ara-C-transformed cell lines. The expression of malignancy in these clones was associated with an excess of 57 chromosomes over 73 chromosomes.

Animals↗
PubMed1975

Malignant transformation of mouse cells by cigarette smoke condensate.

A low-nicotine cigarette smoke condensate, 12 fractions of the condensate, and a reconstituted sample were tested for their ability to induce transformation in the mouse cell line 3H/10T-1/2 CL-8. This cell line is noted for its remarkable low spontaneous rate of transformation. Both the crude condensate and the reconstituted sample as well as two specific fractions induced transformation in the mouse cells. These transformed cells produced fibrosarcomas when injected s.c. into antithymocyte serum-treated syngeneic mice.

Animals↗
PubMed1975

1-beta-D-arabinofuranosylcytosine-induced malignant transformation of hamster and rat cells in culture.

The potent antileukemic chemotherapeutic drug, 1-beta-D-arabinofuranosylcytosine (ara-C), was observed to transform malignantly secondary hamster fetal cells as well as established rat cells in vitro. Results indicated that: (a) hamster cells altered by treatment with ara-C are morphologically indistinguishable from cells transformed with benzo(a)pyrene; (b) the ara-C-induced transformation can be observed under conditions of little or no inhibition of DNA synthesis and little or no cytotoxicity; (c) the transformation can occur with only a 6-hr exposure to ara-C; and (d) the transformation of hamster cells seems to require cellular DNA synthesis for cells in S phase are much more sensitive to ara-C-induced transformation than are G1-arrested cells. Representative transformed colonies of hamster and rat cells produced rapidly growing fibrosarcomas in inoculated newborn hamsters and rats, respectively. Control cells remained nontumorigenic.

Animals↗
PubMed1975

Uptake, metabolism, and persistence of 3-methylcholanthrene in rat embryo cells infected with murine leukemia virus.

The uptake and persistence of 3-methylcholanthrene have been followed in both unifected rat embryo tissue culture cells and in cells infected with type C RNA virus. No significant differences in these parameters were observed as a function of viral infection or cell passage level. Moreover, neither binding of 3-methylcholanthrene to nucleic acids or proteins nor carcinogen metabolism were altered by the viral carrier state. Although transformation of rat cells by chemical carcinogens alone has been reported by us and other authors, the low-passage rat embryo cells used in this study will not transform unless cells are carrying exogenous type C RNA virus. We thus suggest that the virus must play a more direct role in the transformation process rather than affecting the ability of the cell to absorb, retain, or metabolize the chemical.

Animals↗