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S R Sirianni

Publications and source records attributed to S R Sirianni.

16 recordsLinked to original sources
PubMed1990

Comparison of baseline sister-chromatid exchanges (SCE), cyclophosphamide-, ethylnitrosourea (ENU)-induced SCE, ENU-induced cell-cycle delay and chromosome aberrations between Peru and laboratory mice.

The baseline sister-chromatid exchange (SCE) frequency and sensitivity to the effects of the mutagens cyclophosphamide (CPP) and ethylnitrosourea (ENU) in bone-marrow cells of descendants of wild mice trapped from Rimac valley in Peru (Peru mice) were studied and compared to the same effects in laboratory mice. Baseline SCE of the Peru mice were significantly higher than those of the C57BL/6J and DBA/2 mice. The average SCE/cell of 4 Peru mice was 5.4 (range 3.8-7.6), while the average of SCE/cell of either 4 C57BL or 5 DBA mice was 3.2 (range 3.0-3.4). The variation of SCE/cell among Peru mice studied was statistically significant whereas among C57BL or DBA mice it was not. SCE frequencies of primary cultures derived from the ear tissue of 10 Peru (mean SCE/cell = 8.5) were also significantly higher than those of 6 C57BL mice (mean SCE/cell = 7.4). CPP treatment resulted in a dose-dependent increase of SCE frequencies in bone-marrow cells of all the mice. However, some of Peru mice treated with CPP had significantly higher SCE than the other Peru mice and than all of the C57BL and DBA mice treated with equivalent dose. ENU induced increased SCE frequencies in Peru and C57BL mice. Again some of Peru mice either had significantly higher SCE, greater extent induced cell-cycle delay or chromosome aberrations (CA) than other Peru mice and than of all the C57BL mice treated with equivalent dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Comparison of S9 fractions from rats, mice, and Chinese hamsters to metabolize dimethylnitrosamine and diethylnitrosamine to intermediates that induce sister-chromatid exchanges in V79 cells.

This study was designed to compare the ability of hepatic S9 preparations from rats, mice and Chinese hamsters to activate dimethylnitrosamine (DMN) and diethylnitrosamine (DEN) into intermediates capable of causing sister-chromatid exchanges (SCEs) in V79 cells. The results indicated that the hepatic preparations from the species studied differed in their ability to activate DMN while in the case of DEN no species difference in bioactivation was observed. For DMN, a dose-dependent increase of SCEs was seen in cultures treated with various concentrations plus rat, mouse or hamster S9 mix and the mouse S9 mix was the most effective activator of DMN and this was followed by the rat and Chinese hamster S9 mix with little difference noted for the latter 2 species. For DEN, an increase of SCE was seen in cultures treated with various doses plus S9 mix from any of the species studied but unlike DMN, the SCE rate did not increase in a significant dose-dependent manner and no species difference in bioactivation was observed.

Animals↗
PubMed1983

Induction of sister chromatid exchange by various selenium compounds in Chinese hamster cells in the presence and absence of S9 mixture.

This study was designed to investigate the effect of 3 selenium compounds, namely, sodium selenite, sodium selenide and sodium selenate on induction of sister chromatid exchange (SCE) in the Chinese hamster V79 cell line in the presence and absence of S9 mixture. The results indicated that the most potent SCE inducer in the presence of S9 mixture was sodium selenite and this was followed by sodium selenide, while in the absence of S9 mixture the most effective SCE inducer was sodium selenide which was then followed by sodium selenite. For sodium selenate, the data indicated no increase in SCE rate as compared to the control values both in the presence and absence of S9 mixture. In addition, it was observed that growth inhibition as measured by no sister chromatid differentiation or no metaphases was produced by certain doses of the compounds tested. Based on this, the compound that induced the most growth inhibition both in the presence and absence of S9 mixture was sodium selenide and this was followed by sodium selenite. For sodium selenate no growth inhibition was observed. The different capabilities of the selenium compounds tested to induce SCE were clearly demonstrated in the system employed in this study. It is felt that this effect is an important cytogenetic characteristic of these compounds, yet how this activity relates to the antimutagenic and anticarcinogenic properties of these agents is difficult to discern.

Animals↗
PubMed1983

Inhibition of retinoid toxicity by rat liver S9 fraction in cultured mammalian cells.

The effects of retinol (Rol), retinyl acetate (RAc) or retinoic acid (RA) on growth of Chinese hamster V79 cells were studied. In addition, the effect of Rol on cell growth in the human lymphoid cell line RPMI no. 1788 was examined. Cultures were treated with retinoid alone, with retinoid plus S9 mix and with retinoid plus the supernatant of S9 fraction. Treatment of Rol, RAc or RA alone inhibited the growth of both cell lines as evidenced by a dose-dependent decrease of viable cell counts. Concurrent treatment of a retinoid with the well-known metabolic activation system S9 mix containing the rat liver S9 fraction plus enzyme cofactors resulted in a total elimination of the toxic effect of a retinoid. For instance, V79 cells treated with Rol, RAc or RA alone at the highest dose of 32 micrograms/ml, and human lymphoid cells treated with Rol at the highest dose of 24 micrograms/ml resulted in killing of over 90% of the cells, while addition of S9 mix to the cultures treated with such high doses of a retinoid showed no reduction of viable cells as compared with the controls. The supernatant of S9 fraction after high speed centrifugation also had dose-dependent protective effects against the toxicity of retinol in V79 cells. Finally, experiments using sucrose gradient centrifugation and [3H] Rol suggests that binding of a retinoid to its specific binding protein in the S9 mixture and supernatant greatly decreases or abolished the toxicity of free retinoid in cultured mammalian cells.

Animals↗
PubMed1982

Sister-chromatid exchanges and cell-cycle delay in Chinese hamster V79 cells treated with 9 organophosphorus compounds (8 pesticides and 1 defoliant).

Significant increase of sister-chromatid exchanges (SCE) in V79 cells treated with 2 organophosphorus pesticides (OPP), fenthion and oxydemeton-methyl, was observed. The other 7 compounds (6 OPP and 1 defoliant) namely, amaze, azinphos-methyl, bolstar, DEF-defoliant, fensulfothion, monitor and nemacur caused no increase of SCE frequencies at the doses tested. All the compounds except fensulfothion and oxydemeton-methyl induced cell-cycle delay in varying degrees. Cell-cycle delay caused by an OPP was found to be dose-dependent. Based on these data as well as others reported, it would appear that OPP which induce no SCE increase and no or slight cell-cycle delay could be considered as good candidates to substitute the pesticides that have been found to be harmful to the environment.

Animals↗
PubMed1981

Induction of sister-chromatid exchanges and cell cycle delay in cultured mammalian cells treated with eight organophosphorus pesticides.

Induction of sister-chromatid exchanges (SCE) and cell cycle delay in Chinese hamster cell line V79 after treatment with 8 organophosphorus pesticides (OPP) were studied. In addition, these effects were also studied using 1 of the 8 OPP in 2 human lymphoid cell lines. In V79 cells, 6 of the 8 OPP induced significant increase of frequencies of SCE and all the OPP induced various degrees of cell cycle delay. The 6 OPP in decreasing order of SCE induction are methylparathion, demeton, trichlorfon, dimethoate, malathion and methidathion. The 2 OPP that had no effect on SCE are diazion and disyston. The extents of induced cell cycle delay are generally related to the OPP concentrations but does not necessarily correlate with the extent of induction of SCE among the OPP studied. The results of studies on the effect of methyl-parathion on SCE and cell cycle delay in 2 human cell lines showed that both lines had significant and dose-dependent increase of SCE frequencies similar to those observed in V79 cells. In contrast to V79 cells, however, cell cycle delay was not as prominent in the human lines at comparable doses. These studies indicated that 5-bromodeoxyuridine labeling for analyzing SCE and cell cycle delay is a very sensitive method in assessing mutagenic potential of environmental compounds especially those that are highly toxic to and rapidly degradable in mammalian cells such as OPP.

Animals↗
PubMed1981

Effects of retinoids on plating efficiency, sister-chromatid exchange (SCE) and mitomycin-C-induced SCE in cultured Chinese hamster cells.

The effects of 5 retinoids, namely, all-trans-retinol (ROL), all-trans-retinoic acid (RA), all-trans-retinal (RAL), all-trans-retinyl acetate (RAc), and Ro. 10-9359-TMMP ethyl retinoate on plating efficiency, sister-chromatid exchange (SCE) and on mitomycin-C (MMC)-induced SCE were studied in Chinese hamster V79 cells. All the retinoids caused reduction of plating efficiency in a dose-dependent manner but the degree of plating efficiency reduction varied considerably among the retinoids studies. RAL was the most potent reducer of plating efficiency and this was followed in decreasing order by ROL, RAc, RA and Ro. 10-9359. For the effect of various doses of retinoids on SCE, it was clearly demonstrated that addition of each of the 5 retinoids to exponentially growing V79 cells had no significant effect on SCE frequency as compared to the controls. Besides this, these compounds did not alter DCS frequency induced by MMC.

Animals↗
PubMed1981

Studies on osteoporosis. V. Comparison of methods of evaluation of osteoporosis and study of chromosome changes induced by neutron activation.

In vivo activation analysis was compared with ashing and atomic absorption spectrophotometry for the determination of total skeletal calcium content in mice. The results were close to identical. The possible mutagenic-carcinogenic effect of repeated exposure to whole body neutron irradiation was studied by chromosome analysis. Under the conditions of these experiments, no significant chromosome changes were seen.

Activation Analysis↗
PubMed1980

Comparison of induction of sister chromatid exchange, 8-azaguanine- and ouabain-resistant mutants by cyclophosphamide, ifosfamide and 1-(pyridyl-3)-3,3-dimethyltriazene in Chinese hamster cells cultured in diffusion chambers in mice.

Data on induction of sister chromatid exchange (SCE), 8-azaguanine and ouabain-resistant mutants in V79 cells in diffusion chambers in mice treated with three chemicals were compared to determine the relationship between SCE and mutation. For 1-(pyridyl-3)-3,3-dimethyltriazene, a positive, linear correlation was demonstrated between induced SCE and mutation at both loci. For cyclophosphamide and ifosfamide, it was observed that SCE analysis was a more sensitive biological endpoint than induction of mutation.

Animals↗
PubMed1979

Induction of 8-azaguanine- and ouabain-resistant mutants by cyclophosphamide and 1-(pyridyl-3)-3,3-dimethyltriazene in Chinese hamster cells cultured in diffusion chambers in mice.

A host-mediated assay is described for induction of 8-azaguanine-resistant (azgr) and ouabain-resistant (ouar) mutants in Chinese hamster V79 cells cultured in diffusion chambers (DC) in C3H mice. Injection of the hosts with the indirect mutagen/carcinogen cyclophosphamide (CPP) or 1-(pyridyl-3)-3,3-dimethyltriazene (PyDT) caused a dose-dependent increase in mutation frequency at the loci of azgr and ouar in the V79 target cells. Plating efficiency of V79 cells in DC in mice was decreased depending upon the dose of CPP or PyDT given to the hosts. In addition, the relationship between expression time and mutation frequency was examined and discussed. The data support the use of this system as an effective screening procedure for suspected environmental mutagens or carcinogens, especially those that need to be metabolically activated in vivo.

Animals↗
PubMed1978

Sister chromatid exchanges and growth inhibition induced by the flame retardant tris(2,3-dipromopropyl) phosphate in Chinese hamster cells.

The effects of the flame retardant tris(2,3-dibromopropyl) phosphate (Tris-BP) on growth, sister chromatid exchanges (SCE), and chromosome aberrations of Chinese hamster V79 cells cultured either in vitro or in diffusion chambers (DC) implanted into mice were studied. Tris-BP caused a dose- and time-dependent reduction of cell growth as measured by colony-forming activities. A significant dose-dependent increase in SCE was observed in V79 cells either in the cultures treated with Tris-BP or in DC in mice given injections of the chemical. In contrast, Tris-BP in V79 cells in culture, in V79 cells in DC in mice, in two human lymphoid cell lines, or in mouse bone marrow cells in vivo did not significantly increase chromosome aberrations.

Animals↗
PubMed1978

Effect of fungicide Folpet on growth and chromosomes of human lymphoid cell lines.

One normal human lymphoid cell line was treated continuously with the fungicide Folpet (N-trichloromethylthio-phthalimide) at 0.5, 1, 2, and 4 microgram/ml of media and one Burkitt cell line was pulse-treated with the same compound for 15 min at 2.5, 5, 10, and 15 microgram/ml. Various times after treatment, cell viability counts and chromosomes analyses were made. Severe cell growth inhibition and an increase in chromosome aberrations were observed in both cell lines. There were two types of induced chromosome aberrations. Aberrations type A appeared in cultures treated with lower doses and were characterized by chromosome or chromatid gaps and breaks and also infrequently seen exchanges and dicentrics. In the later stages of the experiment, the rate of growth and aberrations returned to control levels. Chromosome aberrations type B appeared in early samples of cultures treated with higher doses. The whole complement of chromosomes was affected. The aberrations included chromosome stickiness, despiralization and pulverization. The cultures died off within two days.

Cell Division↗
PubMed1978

Study on the mutagenicity of conjugated estrogens in human, animal and bacterial systems.

Conjugated estrogens were studied for mutagenicity (and implied carcinogenicity) in two strains of S. typhimurium, two normal and three neoplastic human lymphoid cell lines (the latter from Burkitt's lymphoma patients) in cell culture and a Chinese hamster cell line in diffusion chambers implanted into mice. No significant increase in mutation rate or chromosome aberrations were noticed after exposure to conjugated estrogens.

Animals↗