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The Relationship between Job Stress and Psychosocial Stress among Nurses at a University Hospital
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Hwan Cheol Kim, Keun Sang Kwon, Dai Ha Koh, Jong Han Leem, Sin Goo Park, Joo Youn Shin, Yeui Cheol Lee, Yong Kyu Kim
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Korean Journal of Occupational and Environmental Medicine 2006;18(1):25-34. Published online March 31, 2006
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DOI: https://doi.org/10.35371/kjoem.2006.18.1.25
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 Abstract
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- OBJECTIVES
This cross-sectional study investigated the relationship between job stress and psychosocial stress among nurses at a university hospital in Incheon, Korea.
METHODS
A questionnaire survey was administered to 476 nurses, of which 320 (67.2%) questionnaires were returned and 299 (62.8%) were regarded as containing reliable data for analyses. A structured self-reported questionnaire was used to assess each respondent's sociodemographics, sleep quality, physical burden, job stress and psychosocial stress. Seven domains of occupational stress (e.g., Job demand, Insufficient job control, Interpersonal conflict, Job insecurity, Lack of reward, Organizational system and Occupational climates) according to the Korean Occupational Stress Scale (KOSS) were used and psychosocial stress was measured using Dr. Chang's PWI-SF (Psychosocial Well-being Index-Short Form). We estimated the relation of job stress to psychosocial stress using univariate and logistic regression analyses.
RESULTS
The logistic regression analyses indicated that the groups with high stress in 'Insufficient job control' (OR=2.67, 95% C.I.=1.37-5.23), 'Interpersonal conflict' (OR=2.32, 95% C.I.=1.19-4.51), 'Job insecurity' (OR=2.51, 95% C.I.=1.17-5.36), 'Organizational system' (OR=2.80, 95% C.I.=1.39-5.63), and 'Lack of reward' (OR=2.98, 95% C.I.=1.55-5.74) were more likely to experience high psychosocial stress.
CONCLUSIONS
Our results tend to suggest that job stress is associated with psychosocial stress. The importance of job stress should be acknowledged and stress management programs need to be instigated to minimize the psychosocial stress caused by job stress.
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Citations
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Effects of Selenium on Apoptosis Induced by Methyl Mercury Chloride in RAW 264.7 Cells
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Keun Snag Kwon, Dai Ha Koh, Jung Ho Youm, Wook Hee Yoon
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Korean Journal of Occupational and Environmental Medicine 2003;15(3):237-251. Published online September 30, 2003
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DOI: https://doi.org/10.35371/kjoem.2003.15.3.237
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Abstract
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- OBJECTIVE: This study was performed to evaluate the protective effects of selenium against the methyl mercury chloride (MeHgCl) induced cell apoptosis.
METHODS
The effect of selenium on the MeHgCl induced cell apoptosis was observed in mouse macrophage-derived RAW 264.7 cells, in vitro. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM).
RESULTS
MeHgCl exerted a dose dependent cytotoxicity, as demonstrated by the MTT assay, an assay dependent, in part, on mitochondrial function. Concurrent exposure to selenium provided complete protective effects against the cytotoxicity induced by MeHgCl. Pretreatment with selenium increased the protective effects of subsquent administrations of selenium in conjunction with MeHgCl, but pretreatment of selenium alone did not provide protection against MeHgCl when given alone. Selenium administered after exposure to MeHgCl did not repair the existing MeHgCl induced cytotoxicity.Furthermore, the apoptosis induced by MeHgCl was revealed by the DNA fragmentation, using the terminal deoxynucleotidyl transferase Biotin-dUTP nick end labeling (TUNEL) assay, alterations to the nuclear morphology, by nuclei staining, and the plasma membrane lipid organization, as shown by cell flow cytometry. The apoptosis induced by MeHgCl was prevented by the concurrent exposure to selenium, or pretreatment with selenium, prior to the administration of selenium in conjunction with MeHgCl. However, no inhibittion of the MeHgCl induced apoptosis was observed with selenium pretreatment prior to exposure to MeHgCl alone, or with the administration of selenium after exposure to MeHgCl.
CONCLUSIONS
These results suggest that the coexistence of selenium and MeHgCl are essential for the protective effects of selenium against the MeHgCl-induced apoptosis, and the cytotoxicity, in RAW 264.7 cells, and may involve selenium-MeHgCl binding.
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Effect of Glutathione on Apoptosis Induced by Methyl Mercury Chloride
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Jung Ho Youm, Dai Ha Koh, Keun Sang Kwon, Me Yae Lee
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Korean Journal of Occupational and Environmental Medicine 2002;14(4):377-391. Published online December 31, 2002
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DOI: https://doi.org/10.35371/kjoem.2002.14.4.377
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Abstract
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- OBJECTIVES
This study was performed to evaluate the critical role of glutathione(GSH) in methyl mercury chloride(MeHgCl)induced cell apoptosis.
METHODS
The effect of GSH in MeHgCl induced cell apoptosis was observed in mouse macrophage-derived RAW 264.7 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium(DMEM).
RESULTS
MeHgCl exerted a dose dependent cytotoxicity,as demonstrated by the MTT assay, which is an assay dependent partially on the mitochondrial function. Moreover, in the presence of NAC, a GSH precursor, the MeHgCl induced cytotoxicity was significantly decreased whereas BSO, a specific GSH synthesis inhibitor,increased the MeHgCl induced cytotoxicity.The MeHgCl induced DNA fragmentation and chromatin condensation was consistent with the morphological alterations. The MeHgCl treated cells exhibited increasing annexin V-FITC binding to the phos-phatidylserine(PS)translocated from the inner to the outer leaflet of the plasma membrane and those cells with NAC pretreatment significantly exhibited decreasing annexin V-FITC binding compared to the cells treated with MeHgCl only. However BSO pretreatment markedly exhibited the increasing annexin V-FITC binding. The MeHgCl treated cells generated ROS, which was evidenced by the oxidation of dihydroethidine and the generation of the fluorescent product, ethidium. In addition, BSO pretreatment further enhanced the extent of ROS generation caused by MeHgCl whereas NAC pretreatment decreased the amount of ROS generation. MeHgCl led to a dose dependent decrease in the GSH content. Although MeHgCl exposure significantly reduced the GSH level, those cells that had a NAC pretreatment contained a higher level of GSH compared to the cells treated with MeHgCl only. In contrast, BSO pretreatment futher enhanced the extent of GSH depletion caused by MeHgCl.
CONCLUSIONS
These results indicate that MeHgCl reduced the GSH content and impaired the defense against oxidative damage caused by ROS formation in RAW 264.7 cells. It is possible that these factors leads to the activation of the apoptosis signaling pathway. Ultimately these results suggest that GSH plays a crucial role in protecting the activity against MeHgCl induced apoptosis.
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Induction of Apoptosis by Heavy Metals in HL-60 Cells
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Nam Song Kim, Tae Ho Seong, Kwang Ho Cho, Jung Ho Youm, Dai Ha Koh
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Korean Journal of Occupational and Environmental Medicine 1999;11(4):557-568. Published online December 31, 1999
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DOI: https://doi.org/10.35371/kjoem.1999.11.4.557
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Abstract
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- OBJECTIVES
Apotosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metal are well described, little is known about the mechanism of apoptosis by heavy metal toxicity. This study is designed to define the induction of apoptosis by which heavy metals exert the cytotoxic effect on human promyelocytic leukemic HL-60 cells.
Methods
After the incubation with CdC12, Na2SeO3 and HgC12, viability of the cells were measured by MTT assay. DNA fragmentation was analyzed by electrophoresis. For measurement of caspase 1 and 3-like proteases activity, the whole lysates were subjected to the proteolytic cleavage and then measured by using fluorospectrometry. c-JUN N-terminal kinase (JNK) activity was detected by an in vitro kinase assay. Transcriptional activities of activating protein-1 (AP-1) and nuclear factor-kB (NF-kB) were measured by elec trophoresis mobility shift assay (EMSA).
RESULTS
Cadmium (l2OuiN/I) and selenium (30,iM) induce the apoptosis of HL-60 cells which is characterized by the ladder pattern of DNA fragmentation. Cadmium and selenium induce the activation of caspase-3 in a time dependent manner. They also increase the phosphotransferase activities of c-JUN N-terminal kinase (JNK) in cadmium and selenium treated HL-60 cells. Furthermore, cadmium and selenium increase the activation of transcriptional factors including AP-i and NF-kB.
CONCLUSIONS
These results suggest that cadmium and selenium induce the apoptotic death of HL-60 cells via activation of DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kB.
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A Study of Protective Effect of Selenium Against Cytotoxicity of Methylmercury Chloride
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Dai Ha Koh, Jung Ho Youm, Young Sang Koh, Sun Hwan Joh, Tak Soon Oh
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Korean Journal of Occupational and Environmental Medicine 1998;10(3):310-319. Published online August 31, 1998
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DOI: https://doi.org/10.35371/kjoem.1998.10.3.310
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Abstract
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- The purpose of the present study was to elucidate the cytotoxical influence of mercurial compounds and the protective effect of selenium against mercurial compounds. The effects of mercury compounds and selenium on the syntheses of nitrite(NO2-) and ATP were observed in the cell cultures of EMT-6 cells and peritoneal macrophages from Balb/c mouse. The viabilities of EMT-6 cells and peritoneal macrophages at the end of culture were significantly decreased in dose-dependent manner by methylmercury chloride (CH3HgCl) added into the media. NO2- and ATP syntheses of the cells were dose-dependently inhibited by CH3HgCl. Simultaneous addition of the equimolar dose of selenium completely prevented mercury-induced inhibitions of NO2- and ATP syntheses, which were observed in both of EMT-6 cells and peritoneal macrophages. But these effects of selenium were not appeared in the new medium containing mercurials only which were removed the selenium after the pretreatment of selenium for 6 hours. These results suggest that protective effect of selenium against mercurial compounds was archived by the formation of a complex consisting of Se-Hg or Se-Hg-protein. Though its mechanism was not clear, the protective role of selemium against the mercury toxicity would be exhibited in the immunological system.
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Cytotoxic Influence of Mercurial Compounds and the Protective Effect of Selenium in the EMT-6 Cells
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Jung Ho Youm, Dai Ha Koh, Byoung Yul Soh
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Korean Journal of Occupational and Environmental Medicine 1997;9(3):469-477. Published online October 31, 1997
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DOI: https://doi.org/10.35371/kjoem.1997.9.3.469
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Abstract
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- No abstract available.
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A Study of Cytotoxical Mechanism of Mercurial Compounds in RAW264.7 Cell Line
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Kong Ho Kirn, Byoung Yul Soh, Dai Ha Koh
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Korean Journal of Occupational and Environmental Medicine 1996;8(3):560-569. Published online December 31, 1996
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DOI: https://doi.org/10.35371/kjoem.1996.8.3.560
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Abstract
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- The effects of glucose on the productions of ATP and nitrite which are inhibited by mercury compounds, were examined in a cell culture system of RAW 264.7 cells. The cells were cultured in Dulbecco's Modified Eagle's medium (DMEM) with cytokines, IL-1 and TNF for 24 hours. The viablility of RAW 264.7 cells at the end of culture was significantly decreased by mercury chloride or methylmercury chloride added into the media in dose-dependent manner, however the viability of RAW 264.7 cells were influenced in the concentrations lese than 0.8micrometer of mercury chloride or 0.4micrometer of methylmercury chloride. The addition of 4.5 g/l glucose to normal DMEM lowered the pH of media to the range of 6.7-6.8 after 48 hours of culture, but not for the cell survivals. This supplement of glucose to the media also prevented the inhibitions of ATP and nitrite syntheses which were caused by mercurial compounds. These results suggest that the disorder of cell mediated immunity by mercurials could be related to the inhibition of nitric oxide synthesis which seams to be caused by the inhibition of ATP synthesis, especially related to the citric acid cycle.
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Effect of Mercury Chloride on Peritoneal Macrophage or EMT-6 cell from Balb/c mice
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Dai Ha Koh, Jung Ho Youm, No Suk Ki, Gyung Jae Oh, Kuen Sang Kwon, Sung Yeup Kim, Nam Song Kim
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Korean Journal of Occupational and Environmental Medicine 1996;8(2):201-209. Published online September 30, 1996
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DOI: https://doi.org/10.35371/kjoem.1996.8.2.201
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Abstract
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- The effect of treatment of mercury chloride on the nitrite and nitrate synthesis was observed in peritoneal macrophages from Balb/c mice and EMT-6 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM) with cytokines. Amounts of nitrite and nitrate in the culture media after 24 and 36 hours of culture were about 2-fold, and 3-fold of those measured after 12 hours respectively. There were very close associations between the amounts of nitrite and nitrate measured in the culture media, according to culture time. The survival rate of peritoneal macrophages was significantly decreased by mercury chloride added into the media in dose-dependent manner, however the survivals of EMT-6 cells were not influenced by mercury chloride concentration in media. Nitrite and nitrate syntheses were dose-dependently decreased by mercury chloride added in culture media. These results reported here suggest that the disorder of cell mediated immunity by mercurials could be related to the inhibition of nitric oxide synthesis which seems to be caused by the inhibition of metabolism of cells.
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A Study on Working Environment and Health Status of Workers in Some Dyeing Factories
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No Suk Ki, Chung Ja Ahn, Dai Ha Koh, Jung Sang Lee, Yoo Yong Lee, Jae Hyung Lee, Jung Ho Youm, Yong Il Shin
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Korean Journal of Occupational and Environmental Medicine 1994;6(1):3-16. Published online February 28, 1994
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DOI: https://doi.org/10.35371/kjoem.1994.6.1.3
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Abstract
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- This study was carried out to evaluated the actual conditions of working environment and health status of workers and search more effective health management method of workers in some dyeing factories. This study was conducted from April 1 to October 30, 1992, for 426 workers in two dyeing factories and an electric wire making factories.
Among 324 workers in two dyeing factories, 57.5% were male and 42.5% were female. Most of the engaged workers had less than 2 years of working carrier and aged 30 years or below. The used chemical substances exceeding 1 ton per a month were sodium hydroxide(NaOH), hydrogen peroxide(H2O2), sodium chlorite(NaClO2), sodium sulfate(Ma2SO4), sodium carbonate(Na2CO3), and sodium hydrosulfite(Na2S2O4). The used chemical dyes exceeding 100kg per a month were suncion blue H-ERD, levafix brilliant red E-4BA, suncion yellow E-3G, and remazol black B. As the allowable exposure time by governmental threshold limit valuses to industrial noise levels in 90 dBA for 8 hours. Average noise levels of the individual plants were ranged from 75 to 95 dB (A). The TLV for total cotton dust in 2.0mg/m3. Average cotton-dust concentration in these working environmental air were ranging from 0.2-1.3mg/m3. The TLV chlorine, acetic acid and formic acid are 1 ppm, 10 ppm & 5ppm, respectively. The range of chlorine, and acetic and formic acid concentration in these working environmental air were detected 0.2-1.6 ppm and at trace level. The accident by chemical substances and dyes was not found on these working environment.
From the physical examination and Todai Health Index scores results, there was no significant correlation between the used chemical substances and the diseases, such as bronchial asthma, other hyperreactive respiratory diseases and contact dermatitis. It was suggested that long term survey should be performed to detect the occupational health problem on these working environment.
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