PubMed Health⌕ Search

Biomedical subjects

N C Popescu

Publications and source records attributed to N C Popescu.

At least 145 records · Page 8Linked to original sources
PubMed1982

12-O-tetradecanoyl-phorbol-13-acetate and its relationship to SCE induction in Syrian and Chinese hamster cells.

12-O-Tetradecanoyl-phorbol-13-acetate (TPA) in conditions that produce enhancement of ultraviolet light (UV) and x-irradiation Syrian hamster embryo cell (HEC) transformation did not cause further increase in the sister chromatid exchange (SCE) frequency induced by UV and x-irradiation, two physical carcinogens that differ in their mode of DNA interaction and efficiency of SCE induction. Several factors which might influence SCE induction by TPA were studied on HEC and Chinese hamster V79-4 cells. Heat-inactivated serum was used because of the possibility that a serum component may interfere with TPA ability to cause SCE. TPA effect on SCE was determined at the first and second division post treatment on cells exposed to different 5-bromodeoxyuridine (BrdUrd) concentrations. Independent of BrdUrd concentration (1-10 microgram/ml medium) and the number of cell divisions post treatment TPA (0.01-2 microgram/ml medium) was ineffective in inducing SCE in exponentially and stationary HEC cultures cultivated in medium supplemented with heat-inactivated serum. Also, TPA did not increase the SCE frequency in V79-4 Chinese hamster cells cultured in heat-inactivated or noninactivated serum. Although SCE induction, a cellular response to carcinogen-induced DNA damage, may be important for the induction of transformation by environmental agents, the enhancement of transformation frequency caused by TPA occurs without further DNA alterations involved in SCE formation.

Animals↗
PubMed1982

Cytologic detection of virus-specific DNA by in situ hybridization in Syrian hamster embryo cells transformed by viral or combined chemical and viral treatment.

A series of simian adenovirus 7 (SA7)-transformed Syrian hamster cell lines that had T antigen and produced tumors in neonatal hamsters were examined by radioautography in conjunction with in situ molecular hybridization to determine the extent to which the viral genome is integrated on specific chromosomes and the consequences of such integration on sister chromatid exchange (SCE) frequency. No consistent cytological or chromosomal localization of viral DNA in situ hybridization with viral complementary [3H]RNA was detected, even though all lines had an average of one or two viral genomes per cell by molecular hybridization. The SA7 DNA appears to be inserted randomly among the chromosomes and nuclei.

Animals↗
PubMed1981

Relationship of carcinogen-induced sister chromatid exchange and neoplastic cell transformation.

Sister chromatid exchange (SCE) and morphological transformation induced by five chemical carcinogens, N-acetoxy-2-fluorenyl-acetamide (AcAAF), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS), benzo[a]-pyrene (BP), and cisplatinum(II) diamine dichloride (PT) as well as by X-irradiation were quantified in parallel experiments with cultures of Syrian hamster embryo cells (HEC). Incubation of HEC with 5-bromodeoxyuridine (10(-5)M) for two rounds of replication (24 h) required for SCE visualization neither caused morphological transformation nor altered the transformation frequency induced by carcinogen alone. All chemical carcinogens, but not X-irradiation, produced a dose-dependent increase in SCE and transformation frequency, demonstrating the sensitivity of both assays to carcinogens. The ratios of induced SCE relative to transformation frequency, however, varied with the carcinogen. BP, MMNG, and AcAAF were similarly efficient in inducing SCE compared to transformation but were considerably less effective than MMS and PT. X-irradiation at doses of 200, 300, and 500 R did not cause transformation and induced a low frequency of SCE. On a molar basis, MMS and PT were the most effective in SCE induction relative to transformation, MNNG and AcAAF were less effective, and BP was the least effective carcinogen. The positive linear correlation between chemical carcinogen-induced SCE and transformation suggests a relationship between the two cellular responses.

Acetoxyacetylaminofluorene↗
PubMed1980

Reduced N-methyl-N'-nitro-N-nitrosoguanidine sister chromatid exchange induction in Chinese hamster V79 cells pre-exposed to 5-bromodeoxyuridine.

The sequence in which N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and 5-bromodeoxyuridine (BrdU) are added to cell cultures affects the number of sister chromatid exchanges (SCE) induced by MNNG. When V79 Chinese hamster cell monolayer cultures were treated with MNNG for 2 h prior to addition of BrdUrd, approximately a 4-5-fold increase in SCE was observed at the second division metaphases compared to controls exposed to BrdU alone. This effect was independent of whether one or three DNA strands had been substituted as a result of incubating the cells through one or two DNA synthesis periods in the presence of BrdU. This increase in SCE also occurred after MNNG exposure and BrdU incubation was extended for three division cycles. In contrast, when BrdU incorporation preceded MNNG treatment, the average number of SCE/metaphase was reduced 70-80% at the second division cycle and 60% relative to the total number found in three division cycles. SCE induction by MNNG does not involve a caffeine sensitive step since caffeine had not effect on the SCE frequency regardless of the treatment protocol. The conditions in which BrdU preceded MNNG exposure may be responsible for either reducing the number of DNA sites available for interaction with MNNG or preventing the expression of SCE.

Animals↗
PubMed1980

Antipain inhibits N-methyl-N'-nitro-N-nitrosoguanidine-induced transformation and increases chromosomal aberrations.

The morphologic transformation induced in Syrian hamster embryo cells by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (0.25 microgram/ml of medium) is inhibited by posttreatment with antipain (6-600 microgram/ml), a protease inhibitor, but is unaffected by pretreatment. DNA replication relative to untreated controls is not affected by MNNG, antipain, or the combination of the two; no synergistic lethality of antipain and MNNG occurred as reflected in the cloning efficiency. Antipain was ineffective in influencing MNNG-induced sister chromatid exchanges, but it increased frequencies of chromosomal aberration (per metaphase) at 10, 26, and 40 hr when cells were treated with MNNG at 0.25 microgram/ml of medium followed by antipain 10 min later, the procedure used in the transformation studies. Antipain also increased the average number of aberrations at the second mitosis (34 hr) when the MNNG concentration was doubled. Chromatid exchanges increased 26 hr posttreatment with the combination of MNNG and antipain used for transformation. No difference in MNNG-induced aberrations was observed when antipain preceded MNNG by 24 hr. Although the mode of actin of antipain is unknown, antipain does not inhibit transformation by suppressing chromosomal rearrangements that could convert recessive mutations to the homozygous state.

Animals↗
PubMed1980

Enhancement of N-methyl-N'-nitro-N-nitrosoguanidine transformation of Syrian hamster cells by a phorbol diester is independent of sister chromatid exchanges and chromosome aberrations.

12-O-Tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter, enhances the morphologic transformation of Syrian hamster embryo cells induced by low transforming concentrations of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (0.025-0.1 microgram/ml) without potentiation of cell lethality or of changes in sister chromatid exchanges (SCEs) or chromosomal aberration frequencies. When MNNG was added to logarithmically growing cultures and TPA was added 2, 24, or 48 hr later, no changes in SCE frequency relative to MNNG alone occurred. Similar results were obtained with TPA in cells that had been exposed to MNNG in stationary growth phase. Whereas no transformation occurred with TPA alone and pretreatment with TPA did not affect MNNG transformation, its addition 2 hr after MNNG reduced transformation frequency but addition 24-72 hr after MNNG increased the transformation frequency up to 6-fold. TPA had a minimal effect on increasing the transformation frequency (2-fold) induced by MNNG at 0.25 micrograms/ml, a high concentration. Of three polycyclic hydrocarbons, perylene, benzo[g,h,i]perylene, and benz[a]anthracene, known as weak or noncarcinogens, only benz[a]anthracene induced a very low transformation frequency; however, after TPA, transformation occurred with all three. Because the number of cells whose transformation was initiated by low doses of carcinogen is much larger than the number of cells giving rise to transformed colonies in the absence of TPA, the frequency of the initial event is greater than can be expected from point mutations. Furthermore, the promotional aspect of transformation is not accompanied by a parallel increase in SCE.

Animals↗
PubMed1980

Chromosomal interrelationship of hamster species of the genus Mesocricetus.

The similarity of chromosomes and the mode by which differences occurred in the chromosomes of the species comprising the genus Mesocricetus, M. auratus (2n = 44), two "cryptic" species of M. brandti (2n = 44 and 2n = 42) and M. newtoni (2n = 38) were determined. Most of the autosomes and the sex chromosomes have either complete or partial G-band correspondence and thus provide definitive evidence for the taxonomic relationship of these species. The karyotypic differences occurred primarily as a result of deletion of sex chromosome heterochromatin and of autosomal translocations that frequently involved chromosomes with heterochromatic short arms or chromosomes bearing NOR's. Only one Robertsonian centric fusion occurred. Despite the conservatism of arrangement of the genetic material, the chromosomal distribution of heterochromatin diverged during the evolution of these species. M. brandti and newtoni each have a metacentric chromosome with a common long arm matching a submetacentric M. auratus autosome, but a short arm corresponding to two different M. auratus chromosomes. These translocations are crucial for explaining the direction of chromosomal evolution of these species and indicate that M. auratus was the commmon ancestral species and that M. brandti and newtoni subsequently evolved independently.

Animals↗
PubMed1979

Cis-platinum(II) diamine dichloride causes mutation, transformation, and sister-chromatid exchanges in cultured mammalian cells.

The anti-tumor agent cis-platinum(II) diamine dichloride caused dose-dependent toxicity in V79 Chinese hamster cells and in secondary Syrian hamster embryo cells. Chromosome aberrations were induced and positive dose--response relationships were observed for induction of sister-chromatid exchanges and 6-thioguanine-resistant mutations in V79 cells and morphologic transformation of secondary Syrian hamster embryo cells. The findings suggest that this chemical is a potential human carcinogen.

Animals↗
PubMed1979

Heterogeneity of constitutive heterochromatin in somatic Syrian hamster chromosomes.

Syrian hamster constitutive heterochromatin was analyzed for C-band distribution and for BrU late-replication pattern. Characteristic for this species is relatively large amounts of sex-chromosome and autosomal heterochromatin. The distribution of constitutive heterochromatin was determined. The long term of the X chromosome, the whole Y, the short arms of 8 autosomal pairs, the long arm of the smallest metacentric pair, and the centromeric regions of 12 pairs stained intensely dark on C-band preparations. In contrast to the heterochromatin in the centromeric regions, the autosomal short-arm heterochromatin has an increased susceptibility to the denaturation process, as indicated by prolonged exposure to NaOH or Ba(OH)2. Such further exposure to denaturing agents results in an intense dark stain only on the sex-chromosome heterochromatin and centromeric regions of the autosomes. The BrdU late-replication pattern demonstrated that the late-replicating regions correspond to C-bands. Centromeric regions replicate late in the S phase; however, no centromeric region is among the latest replicating segments of the complement. Centromeric and noncentromeric heterochromatin are two distinct categories of constitutive heterochromatin.

Animals↗
PubMed1977

Vulnerability of specific rat chromosomes to in vitro chemically induced damage.

The treatment of rat embryo secondary cultures with DMBA or DMBA-3H for 5, 9, or 24 h resulted in chromosome damage consisting mainly of chromatid type aberrations. There was an increase in the percentage of labelled nuclei and metaphases with increasing length of exposure. In terms of incidence of chromatid lesions, the largest telocentric chromosome (No. 2) was the most susceptible of the autosomes. Banding pattern analysis demonstrated that the region associated with negative band 2q24 of the No. 2 chromosome had the highest number of lesions. An increased accumulation of DMBA-3H label occurred in approximately the same chromatid area of a small fraction of cells exposed for either 5 or 9 h prior to mitosis. The complete loss of DMBA-3H chromosomal labelling after DNAse treatment suggests that the visible grains represent carcinogen-bound DNA. After DMBA and BrdUrd, there was an increase in the number of sister chromatid exchanges compared to controls treated with BrdUrd only; the location of the exchange points on chromosome No. 2 was similar in samples treated with either DMBA and BrdUrd or BrdUrd alone. Additional experiments with thymidine-3H showed that the non-random chromatid lesions on chromosome No. 2 may result from endogenous radiation from the incorporated tritium. These studies demonstrate that a specific chromosome may be affected by diverse agents and that chromatid lesions frequently occur at the site of sister chromatid exchanges.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Banding pattern analysis of initial structural chromosome alterations induced by n-methyl-n'-nitro-n-nitrosoguanidine in Syrian hamster cells.

Cultured secondary Syrian hamster embryo cells exposed to 0.5 N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) microgram/ml medium exhibited chromatid type of aberrations consisting of gaps, breaks and exchanges. Although no specific chromosome or chromosome segment was preferentially affected, chromosomes belonging to the larger groups tended to more often involved. G-band analysis demonstrated that 80% of the lesions occurred in negative bands, 9% involved the centromere, 3% were on non-banded heterochromatin, and approximately 8% of the lesions could not be definitely categorized by G-band analysis. Whether the lesions occur at positive bands or at the interface between negative and positive bands is difficult to discern by the G-band resolution. The Y chromosome compared to autosomes of similar size rarely had lesions. X chromosome damage was found in both the euchromatic and heterochromatic arms. However, both sex chromosomes, as well as an autosome (E20) which is heterochromatic on its long arm, were not found joined to the chromatids of other chromosomes, further emphasizing that chromosomes with large heterochromatic areas are isolated in terms of chromatid exchange events. The analysis of MNNG induced chromosome damage indicates that the negative bands are the primary site of damage and points of exchange.

Azure Stains↗
PubMed1977

Sister chromatid exchange and chromosome aberration analysis with the use of several carcinogens and noncarcinogens.

Several chemical carcinogens and noncarcinogens were tested for their ability to induce sister chromatid exchanges (SCE) and structural chromosome aberrations in cultured V79-4 Chinese hamster cells. All of the direct-acting carcinogens induced a large increase in SCE frequency. Two chemicals, which are mutagenic in microorganisms but whose carcinogenicity is poorly documented, also increased the frequency of SCE. Carcinogenic polycyclic hydrocarbons caused an increased incidence of SCE only when a metabolizing feeder layer was used, whereas no increase was observed with noncarcinogenic polycyclic hydrocarbons. The other noncarcinogens also did not influence the SCE frequency. Although some chemicals increased the frequency of structural chromosome aberrations, no correlation was found between the frequencies of SCE and aberrations.

2-Acetylaminofluorene↗
PubMed1976

Chromosome patterns (G and C bands) of in vitro chemical carcinogen-transformed guinea pig cells.

The chromosomes of five chemical carcinogen-transformed strain 2 guinea pig fetal cell lines were identified by G and C banding techniques and were compared with the normal karyotype from secondary untreated cultures. One line transformed by benzo(a)pyrene had a diploid constitution with no G and C band alterations. Three lines were near diploid, one was near tetraploid, and each contained abnormal chromosomes. A 3-methylcholanthrene line had an abnormal metacentric chromosome formed by centric fusion of two nonhomologous autosomes. The three N-methyl-N'-nitrosoguanidine or diethylnitrosamine cell lines exhibited submetacentric or subtelocentric abnormal chromosomes originating from translocations between two No. 1 or a No. 1 and another autosome. The involvement of Chromosome 1 may be due to its association with nucleolar organization. The greater frequency of contact between such chromosomes, compared to other autosomes, creates an increased risk of chromatid exchange possibly explaining their frequent participation in abnormal chromosome formation or nondisjunction.

Benzopyrenes↗