No abstract available.
Anemia* ; Chromatids* ; Humans ; Siblings*

When cells are exposed to low doses of a mutagenic or clastogenic agents, they often become less sensitive to the effects of a higher does administered subsequently. Such adaptive responses were first described in Escherichia coli and mammalian cells to low doses of an alkylating agent. Since most of the studies have been carried out with human lymphocytes, it is urgently necessary to study this effect in different cellular systems. Its relation with inherent cellular radiosensitivity and underlying mechanism also remain to be answered. In this study, adaptive response by 1 cGy of gamma rays was investigated in three human lymphoblastoid cell lines which were derived from ataxia telangiectasia homozygote, ataxia telangiectasia heterozygote, and normal individual. Experiments were carried out by delivering 1 cGy followed by 50 cGy of gamma radiation and chromatid breaks were scored as an endpoint. The results indicate that prior exposure to 1 cGy of gamma rays reduces the number of chromatid breaks induced by subsequent higher does (50 cGy). The expression of this adaptive response was similar among three cell lines despite of their different radiosensitivity. When 3-aminobenzamide, an inhibitor of poly (ADP-ribose) polymerase, was added after 50 cGy, adaptive responses were abolished in all the tested cell lines. Therefore it is suggested that the adaptive response can be observed in human lymphoblastoid cell lines. Which was first documented through this study. The expression of adaptive response was similar among the cell lines regardless of their radiosensitivity. The elimination of the adaptive response by 3-aminobenzamide is consistent with the proposal that this adaptive response is the result of the induction of a certain chromosomal repair mechanism.
Ataxia Telangiectasia ; Cell Line* ; Chromatids ; Escherichia coli ; Gamma Rays* ; Heterozygote ; Homozygote ; Humans* ; Lymphocytes ; Radiation Tolerance

Sister chromatid exchanges(SCEs) and cell cycle kinetics were proposed as a sensitive and quantitative assay for mutagenicity and cytotoxicity in short-term cultures of phytohemagglutinin(PHA)-stimulated human lymphocytes. Therefore, this study was performed to investigate the relation between the cytotoxic effects and sister chromatid exchanges. The results are summarized as follows: 1) The frequency of SCEs per cell are 13.1+/-2.8 in the lower concentration of 6.25x10(-9) M and 75.8+/-8.2 in the highest concentration of 1.00+/-10(-7) M. Mitotic index is decreased in the higher concentration of mitomycin C. The result indicates that mitomycin C led to a dose dependent increase in SCE frequency, but decrease in mitotic index. 2) Chromosomal analysis was performed on metaphase cells that have divided one, two, and three or more times for cell cycle kinetics by fluorescence-plus-Giemsa(FPG) technique. According to the increased but the cells of third division are greatly decreased. 3) The frequency of SCEs per chromosome by chromocomal group are decreased gradually from A group to G group. But relationships between specific chromosomal group and SCEs frequency are not found.
Cell Cycle ; Chromatids ; Humans ; Humans* ; Kinetics ; Lymphocytes ; Metaphase ; Mitomycin* ; Mitotic Index ; Siblings* ; Sister Chromatid Exchange*

In understanding radiosensitivity a new concept of inherent radiosensitivity based on individuality and heterogeneity within a population has recently beer explored. There has been some discussion of possible mechanism underlying differences in radiosensitivity between cells. Ataxia telangiectasia(AT), a rare autosomal recessive genetic disorder, is characterized by hypersensitivity to lonizing radiation and other DNA damaging agents at the cellular level. There have been a lot of efforts to describe the cause of this hypersensitivity to radiation. At the cellular level, chromosome repair kinetics study would be an appropriate approach. The purpose of this study was to better understand radiosensitivity in an approach to investigate kinetics of induction and repair of G2 chromatic breaks using normal, AT heterozygous(ATH), and AT homozygous lymphoblastoid cell lines. In an attempt to estimate initial damage, 9-betaD-arabinosyl-2-fluoroadenine, an inhibitor of DNA synthesis and repair, was used in this study. It was found from this study that radiation induces higher chromatid breaks in AT than in normal and ATH cells. There was no significant differences of initial chromatid breaks between normal and ATH cells. Repair kinetics was the same for all. So the higher level of breaks in AT G2 cells is thought to be a reflection of the increased initial damage. The amount of initial damage correlated well with survival fraction at 2 Gy of cell survival curve following radiation. Therefore, the difference of radiosensitivity in terms of G2 chromosomal sensitivity is thought to result from the difference of initial damage.
Ataxia ; Beer ; Cell Line ; Cell Survival ; Chromatids ; DNA ; Humans* ; Hypersensitivity ; Individuality ; Kinetics* ; Population Characteristics ; Radiation Tolerance

Chemotherapy agents can induce chromosomal instability, including a variety of chromatid or chromosomal aberrations. However, only limited data is available on the effect of chemotherapy on the kinetics of chromosomal instability in peripheral blood lymphocytes. Here, we report the case of an ovarian cancer patient who showed chromosomal instability in peripheral blood lymphocytes while undergoing chemotherapy. Karyotypic analysis of peripheral blood 1 day after administration of cisplatin and etoposide showed chromosomal or chromatid aberrations, including gaps, breaks, and fragmentation. Chromosome study after completion of the first chemotherapy cycle showed normal karyotype. This finding suggests that chemotherapeutic agents can induce transient chromosomal instability in peripheral blood lymphocytes.
Chromatids ; Chromosomal Instability ; Chromosome Aberrations ; Cisplatin ; Etoposide ; Humans ; Karyotype ; Kinetics ; Lymphocytes ; Ovarian Neoplasms

In order to evaluate the cytogenetic hazard among hospital workers potentially exposed to low dose of radiation, the analysis of chromosome aberrations(CA) and sister chromatid exchanges(SCE) in lymphocytes were performed in 79 hospital workers and 79 non-exposed workers. The mean frequency of chromosomal exchange and deletion(respectively, 0.20X10-2/cell and 0.39X10(-2)/cell) in the exposed group were significantly higher than those(0.07X10(-2)/cell and 0.23X10-2/cell) in control group. The frequency of sister chromatid exchanges was 5.04/cell in the control vs. 6.57/cell in the exposed group. There were also significant differences in the mean frequencies of CA and SCE adjusted for age, sex, smoking, drinking between two groups. There were no evidence of significant increase of CA and SCE according to the department or duration of employment. But the frequency of cells having chromosome aberration was significantly higher in the exposed group than in the control group related to duration of employment. There was no dose-effect relationship between the cumulative doses and the frequency of CA and SCE. But in the case of last 1 yr cumulative dose, there were evidence of significant dose-dependant increase of chromosome type CA and percentage of cells with aberration. The result suggest that there is cytogenetic hazard in risk group like hospital workers handling low dose radiation. And the analysis CA and SCE are useful biological indicators for the exposure of low dose level of radiation.
Chromatids ; Chromosome Aberrations* ; Cytogenetics ; Drinking ; Employment ; Humans ; Lymphocytes ; Siblings* ; Sister Chromatid Exchange* ; Smoke ; Smoking

Aneuploidy is an important point at issue in human reproductive biology, accounting for both a major proportion of miscarriages and various congenital malformation syndromes among newborns. Despite its high incidence and severe clinical consequences, very little is known about how aneuploidy originates in human. On the other hand, remarkable progress has been made in the research of meiosis. The failure of any process in meiosis can result in chromosome mal-disjunction. The alteration in recombination and the premature separation of sister chromatids are two important processes on which more intensive researches have been done. In addition, mtDNA mutation and sexual dimorphism in aneuploidy genesis have also attracted more and more researchers' attention.
Aneuploidy ; Animals ; Chromatids ; metabolism ; DNA, Mitochondrial ; genetics ; Humans ; Recombination, Genetic ; Sex Characteristics

The chromosomal aneuploidy in oocytes is one of main causes of abortion and neonatal birth defects.It is mainly due to the premature separation of sister chromatid caused by the loss of Cohesin protein complex and the non-disjunction sister chromatids caused by abnormal microtubule dynamics aneuploidy.As a pathway of protein post-translational modification,SUMO modification(or SUMOylation)involves many physiological regulation processes including cell proliferation,differentiation,apoptosis,and cycle regulation.In the oocytes,SUMOylation can regulate the localization of Cohesin protein complex on the chromosome to affect the chromosomal aneuploidy in oocytes caused by premature separation of sister chromatid.On the other hand,SUMOylation can regulate the microtubule dynamics to affect the chromosomal aneuploidy in oocytes caused by non-disjunction sister chromatids.Therefore,SUMOylation plays an important role in regulating the chromosomal aneuploidy of oocytes;the exact mechanisms via which the SUMOylated substrates affect aneuploidy in oocytes remain unclear.This articles reviews the roles of SUMOylation in premature separation and non-isolated chromatid aneuploidy in oocyte from the effects of SUMOylationon Cohesin protein complex and microtubule dynamics.
Aneuploidy ; Cell Cycle Proteins ; Chromatids ; Chromosomal Proteins, Non-Histone ; Chromosome Segregation ; Humans ; Microtubules ; Oocytes ; cytology ; Sumoylation

INTRODUCTION: Chromosomal mutations are casual events in neoplasia development. Biomarker cytogenetic assays can determine exposure to mutagenic agents in occupational settings. This study assessed early biological marker chromosomal aberrations among health workers in the chemotheraphy oncology wards/ clinics, exploring its association to the subjects' occupational, environmental and baseline profile.
METHODS: This was an IRB approved cross-sectional exploratory study among hospital personnel working in the chemotherapy oncology facility of a tertiary government hospital, who underwent structured interview and blood extraction for cytogenetic assay after informed consent. Study funds only permitted assay of 44 specimens of 144 planned sample size, hence, Stata 6.0 only analyzed data from 44 subjects.
RESULTS: All 44 subjects had varying exposure to chemotherapy drug infusions. Of these, 79% had 1.0 breaks per cell (hypersensitive). Predominantly chromatid breaks (CTB), chromatid gaps (CTG), sister chromatid exhanges (SCE) were seen. No significant association was shown between mutagenic sensitivity and baseline characteristics, but with small sample size.
CONCLUSION: 21% borderline to hypersensitive mutagenic sensitivity among oncology workers at the tertiary government hospital is relatively significant, despite small sample size, connoting a must preventive promotive practice of chemotherapy administration in the workplace.

Human ; Male ; Female ; Chromosome Aberrations ; Chromosomes ; Drug Therapy ; Personnel, Hospital ; Cytogenetics ; Chromatids ; Mutagens

Adult ; Chromatids/genetics* ; Chromosome Aberrations ; Humans ; Infertility, Male/genetics* ; Male ; Meiosis ; Metaphase/genetics* ; Spermatocytes/physiology*