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This study was designed to construct and identify the subtracted cDNA library in peripheral blood cells of BALB/c mice and tracheal-bronchial epithelial cells of Wistar rats following exposure to radon inhalation. Two groups of the animals were exposed in a radon chamber at an accumulative dose of 100 WLM, while control animals were housed in a room at a background dose of 1 WLM. To construct a subtracted cDNA library enriched with differentially expressed genes, the SMART technique and suppression subtractive hybridization (SSH) assay were performed. The obtained forward and reverse cDNA fragments were directly inserted into a pMD-18 vector and transformed into Escherichia coli JM109. In total, 593 white bacterial clones were selected from both forward- and reverse-subtracted libraries. Among them, 81 clones were chosen for their differential expressions based on reverse Northern blot. Portions of these cDNA clones were also verified by a quantitative real-time polymerase chain reaction (PCR). The screening resulted in 14 upregulative and 8 downregulative known function/annotation genes, which were revealed to be functionally related to cell proliferation, cell oxidative and DNA damage, apoptosis, and tumor promotion. Access numbers were obtained from the GenBank for 11 unknown expressed sequence tags (EST). Analysis of biological roles of these cDNA fragments may provide further insight into mechanisms underlying adverse molecular events induced by high-dose radon exposure. [ABSTRACT FROM AUTHOR]

Exposure of humans simultaneously to microwave and γ-ray irradiation may be a commonly encountered phenomenon. In a previous study data showed that low-dose microwave radiation increased the survival rate of mice irradiated with 8Gy γ-ray; however, the mechanisms underlying these findings remain unclear. Consequently, studies were undertaken to examine the effects of microwave exposure on hematopoietic system adversely altered by γ-ray irradiation in mice. Preexposure to low-dose microwaves attenuated the damage produced by γ-ray irradiation as evidenced by less severe pathological alterations in bone marrow and spleen. The protective effects of microwaves were postulated to be due to up-expression of some hematopoietic growth factors, stimulation of proliferation of the granulocyte-macrophages in bone marrow, and inhibition of the γ-ray induced suppression of hematopoietic stem cells/hematopoietic progenitor cells. Data thus indicate that prior exposure to microwaves may be beneficial in providing protection against injuries produced by γ-ray on the hematopoietic system in mice. [ABSTRACT FROM AUTHOR]

This study examined the protein expression in lung tissues of rats exposed to radon and cigarette smoke using a proteomic approach. Male Wistar rats were exposed daily to radon at a concentration of 100,000 Bq/m3 for 16 h, and then exposed to 20% cigarette smoke for 1 h for a period of 75 d, with the radon cumulative dose reaching 200 WLM (working level months). Proteins from rat lung tissue were separated by two-dimensional gel electrophoresis (2-DE), stained with Coomassie blue, and analyzed with ImageMaster two-dimensional (2D) platinum software. Differentially expressed proteins were analyzed by matrix-assisted laser desorption/ionization (MALDI) mass spectrometry (MALDI-time of flight [TOF] MS or MALDI TOF/TOF-MS). Twenty prominent proteins that were correlated with signal transduction, metabolism, heat shock and stress, and cytoskeleton construction were identified. Some of the differential expression proteins were verified by Western blot analysis and immunohistochemical staining, and the results were consistent with 2-DE analysis. The identified proteins and peptides might be potential diagnostic markers of lung impairment induced by radon and cigarette smoke exposure. [ABSTRACT FROM AUTHOR]

Mobile phones are widely used globally. However, the biological effects due to exposure to electromagnetic fields (EMF) produced by mobile phones are largely unknown. Environmental and occupational exposure of humans to γ-rays is a biologically relevant phenomenon. Consequently studies were undertaken to examine the interactions between γ-rays and EMF on human health. In this study, exposure to 900-MHz EMF expanded γ-ray damage to SHG44 cells. Preexposure EMF enhanced the decrease in cell proliferation induced by γ-ray irradiation and the rate of apoptosis. The combination of EMF and γ-ray exposure resulted in a synergistic effect by triggering stress response, which increased reactive oxygen species, but the expression of hsp70 at both mRNA and protein levels remained unaltered. Data indicate that the adverse effects of γ-rays on cellular functions are strengthened by EMF. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the differential expression of proteins in lung of rats following long-term exposure to radon. The total proteins of lung tissue from Wistar rats exposed to radon for cumulative doses up to 100, 200, or 400 WLM (working level months) were isolated by two-dimensional electrophoresis (2-DE) and analyzed with ImageMaster 2D Platinum software. Comparison of the 2-DE images between the control and radon-exposed groups resulted in 14 upregulated and 9 downregulated protein spots, of which 15 were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) or matrix-assisted laser desorption/ionization time-of-flight/time-of-flight mass spectrometry (MALDI-TOF/TOF-MS). The simultaneous up-expressions of RAGE and S100A6 indicated that both proteins might be applied as biomarkers for lung injury induced by long-term radon exposure. [ABSTRACT FROM AUTHOR]

This study was designed to screen for differential expression genes in bone marrow cells of mice exposed to radon inhalation. Based upon established pathological findings in mouse, differential screening of gene expressions was conducted by using the SSH method. Among 285 cDNA clones selected from both forward- and reverse subtracted libraries, 45 were chosen for their differential expressions based on reverse Northern blot and quantitative real-time PCR analysis. Of these, up-regulation of the mRNA levels of E-cadherin and down-regulation of the replication protein A1 (RPA1) and casein kinase 1 delta (CKI delta) were also verified by a quantitative real-time PCR. Biological roles of these obtained cDNAs are described and the results of the screening may provide important clues for further investigations of the adverse molecular events induced by radon exposure. [ABSTRACT FROM AUTHOR]