Topic
Sister chromatid exchange
About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.
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TL;DR: The present observation on the effect of chronic low doses of I-131 and Tc-99m indicates the possibility of genotoxic implications of this type of occupational exposure, and personnel who work in nuclear medicine departments should carefully apply the radiation protection procedures.
Abstract: Objective : The aim of this study was to assess whether occupational exposure to chronic, low doses of Iodine 131 (I-131) and Technetium 99m (Tc-99m) may lead to genotoxicity. Medical personnel occupied in nuclear medicine departments are occupationally exposed to low doses of I-131 and Tc-99m. The determination of the frequency of sister chromatid exchanges (SCEs) and of cells with a high frequency of SCEs (HFC) is considered to be a sensitive indicator for detecting genotoxic potential of mutagenic and carcinogenic agents. Therefore, we examined peripheral lymphocytes from nuclear medicine physicians for the presence of both SCE and HFC. Methods : Sixteen exposed nuclear medicine physicians (non-smokers) were compared to 16 physicians (non-smokers) who had not been exposed to chemical or physical mutagens in their usual working environment at the same hospital. Results : A statistically significant difference was found between SCE frequencies and HFC percentages measured in lymphocytes from the exposed and control groups. Conclusions : The present observation on the effect of chronic low doses of I-131 and Tc-99m indicates the possibility of genotoxic implications of this type of occupational exposure. Hence, the personnel who work in nuclear medicine departments should carefully apply the radiation protection procedures and should minimize, as low as possible, radiation exposure to avoid possible genotoxic effects.
33 citations
TL;DR: Cells from blood taken from patients who had been given 8-methoxypsoralen orally 2 h before and then irradiated with UV-A in vitro were found to have an increased exchange rate which could be related to the presence of the drug in the peripheral circulation.
Abstract: Sister chromatid exchange rates in cultured cells from the blood of patients receiving photochemotherapy have been examined as an indicator of possible genetic hazards of the treatment to patients with psoriasis. Lymphocytes of untreated patients with psoriasis appear to have sister chromatid exchange rates after 72 h of culture indistinguishable from normal subjects and there is no evidence from these studies that sister chromatid exchanges are significantly increased in the lymphocytes of patients receiving photochemotherapy. Cells from blood taken from patients who had been given 8-methoxypsoralen orally 2 h before and then irradiated with UV-A in vitro were found to have an increased exchange rate which could be related to the presence of the drug in the peripheral circulation.
33 citations
TL;DR: Modulated cell cycle kinetics of various cell types, stimulate production of reactive oxygen species, and induce keratinocytes to produce interleukin-8 are determined to suggest that induction of IL-8 production is not always the inevitable result of cell cycle perturbations or genetic damage.
Abstract: Tumor promoters, proinflammatory cytokines, endotoxins, and protein synthesis inhibitors can modulate cell cycle kinetics of various cell types, stimulate production of reactive oxygen species, and induce keratinocytes to produce interleukin-8 (IL-8), a potent chemotactant for polymorphonuclear neutrophils and T lymphocytes. The aim of this study was to determine whether perturbations of cytogenetic responses correlated with the induction of IL-8 expression. Cultures of primary human keratinocytes were grown in serum-free medium with 5 μmol/L bromodeoxyuridine to label DNA and exposed either to phorbol-13-myristate-12-acetate (PMA) (0.0001–100 ng/ml), cycloheximice (CHX) (0.01–50 μg), lipopolysaccharide (0.1–100 μg/ml), tumor necrosis factor-α (TNFα) (3.13–50 ng/ml), or interleukin-1α (IL-1α) (1–182 pg/ml). Metaphase chromosome preparations were stained by a fluorescence-plus-Giemsa technique to differentiate sister chromatids. For IL-8 production, keratinocytes were grown to 70% confluency and then exposed to chemicals for 24 h. Immunoreactive IL-8 was quantitated from the supernatants by ELISA. With the exception of benzo(a)pyrene used as a positive control, none of the agents induced sister chromatid exchanges. However, PMA and TNFα induced IL-8 production that coincided with significant cell cycle inhibition. IL-1α had no effect on cytogenetic endpoints, yet stimulated a 6.3-fold increase in IL-8. CHX inhibited cell cycle progression and mitotic activity at concentrations that were 200 times lower than required for IL-8 induction; however, puromycin (0.31–10 μg/ml), another protein synthesis inhibitor, did not induce IL-8. At all concentrations tested, TNFα reduced the mitotic index by ∼45%, slowed cell cycle progression by ∼3.5 h, and induced a flat, albeit large, IL-8 response at concentrations ≥12.5 ng/ml. These agent-specific response patterns suggest that induction of IL-8 production is not always the inevitable result of cell cycle perturbations or genetic damage.
33 citations
TL;DR: A new approach is described for the detection of fetal DNA damage through the enumeration of sister chromatid exchanges (SCE) in mouse fetal chromosomes through reciprocal exchanges of fluorescent intensities.
Abstract: FETAL exposure to agents which damage DNA can result in birth anomalies, cancer and inherited abnormalities. In the present report we describe a new approach for the detection of fetal DNA damage through the enumeration of sister chromatid exchanges (SCE) in mouse fetal chromosomes. SCE can be identified as reciprocal exchanges of fluorescent intensities betweeen sister chromatids in metaphase cells which have divided twice in the presence of bromodeoxyuride (BrdU) (Fig. 1). Analysis of SCE has been shown to be a sensitive and reproducible means of detecting chemical mutagens and carcinogens1–9.
33 citations
TL;DR: Technical grade fenvalerate may be considered as a weak clastogen and a potent inducer of SCEs in mice with certain reservations to possible impurities.
Abstract: Fenvalerate, a synthetic pyrethroid insecticide, is commonly used in agriculture and other domestic applications due to its high insecticidal activity and low mammalian-, avian- and phyto-toxicities However, the genotoxic effect of fenvalerate is highly equivocal In the present study the genotoxic effects of fenvalerate was evaluated using structural chromosome aberration (CA) and sister chromatid exchange (SCE) assays in mice Out of the three doses (5, 10 and 20 mg/kg) tested, statistically significant increase in CA was found following intra peritoneal (ip) treatment of 20 mg/kg of fenvalerate for 24 h (P 5×4 mg / kg ) of fenvalerate could induce any significant effect All the three acute doses induced significant increase in the frequency of SCEs (P
33 citations