Annals of Occupational and Environmental Medicine

Keun Sang Kwon

4 Articles

The Relationship between Job Stress and Psychosocial Stress among Nurses at a University Hospital: Hwan Cheol Kim, Keun Sang Kwon, Dai Ha Koh, Jong Han Leem, Sin Goo Park, Joo Youn Shin, Yeui Cheol Lee, Yong Kyu Kim; Korean Journal of Occupational and Environmental Medicine 2006;18(1):25-34. Published online March 31, 2006; DOI: https://doi.org/10.35371/kjoem.2006.18.1.25

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.

Citations

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Young-Sook Yook, Kiyoshi Sanada
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Factors Affecting the Mental Health of University Hospital Nurses
Sung-Ja Yoon, Ju-Hee Hwang, Eun-Ha Park, Myeong-Hui Choe
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Impact of Psychosocial Factors on Occurrence of Medication Errors among Tehran Public Hospitals Nurses by Evaluating the Balance between Effort and Reward
Tahere Yeke Zaree, Jalil Nazari, Mohhamad Asghary Jafarabadi, Tahereh Alinia
Safety and Health at Work.2018; 9(4): 447. CrossRef
Relationship of Sleep Quality, Physical Stress, Psychological Stress, and Job Stress among Residents
So-Young Yoo, Young-Ah Choi, Young-Kyu Park, Sung-Min Cho, Kyung-Shik Lee, Ga-Young Joo, Hyun Keun Lee
Korean Journal of Health Promotion.2017; 17(1): 9. CrossRef
The impact of long working hours on psychosocial stress response among white-collar workers
Kyungjin LEE, Chunhui SUH, Jong-Eun KIM, Jae Oh PARK
INDUSTRIAL HEALTH.2017; 55(1): 46. CrossRef
The Effect of Empathy on the Job Stress among Nurses
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Journal of the Korea Academia-Industrial cooperation Society.2015; 16(6): 3911. CrossRef
Effects of Emotional Labor and Self-efficacy on Psychosocial Stress of Nurses
Jeong Hee Kim, Young Suk Park
Journal of Korean Academy of Nursing Administration.2015; 21(1): 111. CrossRef
The Effects of Job Stress and Psychosocial Stress among Dental Hygienists
Young-Soon Won, Han-Na Oh
Journal of dental hygiene science.2015; 15(5): 679. CrossRef
Influence of Sleep Quality, Depression and Fatigue on Job stress of Geriatric Hospital Workers
Eun-Hee Hwang
Journal of the Korea Academia-Industrial cooperation Society.2015; 16(8): 5413. CrossRef
The relationships between dietary behavior and health related factors according to shift work in nurses
Ji-Myung Kim, Bok-Hee Kang
Journal of Nutrition and Health.2014; 47(6): 416. CrossRef
Relationship Between Job Stress and Turnover Intention Among Nurses in University Hospitals
Hyun-Ran Shin, Young-Chae Cho
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E ffect of Nitric Oxide (NO) or Hydrogen Peroxide (H2O2) in the Nickel Induced cytotoxicity in RAW 264.7 Cell: Gyung Jae Oh, Keun Sang Kwon; Korean Journal of Occupational and Environmental Medicine 2003;15(1):61-71. Published online March 31, 2003; DOI: https://doi.org/10.35371/kjoem.2003.15.1.61

Abstract PDF: OBJECTIVES
Nickel (Ni) is present in many industrial working environments and consumer products, and is one of the leading cause of allergic contact dermatitis, which is a typical delayed (type IV) hypersensitivity reaction. However, the mechanism by which nickel causes this pathology is not well known. The contact dermatitis induced by nickel is mediated, primarily, through macrophages. This property was similar to autotoxicity related nitric oxide (NO) production. NO mediated cytotoxicity was dependent on both H2O2 and peroxynitrite (OONO-). The purpose of this study was to elucidate the role of NO/H2O2 in the cytotoxicity induced by nickel. Therefore, this study was designed to examine whether nickel could modulate NO/H2O2 production and how the Ni may affect ATP production, intracellular GSH level, and cell viability.
METHODS
This study was based on the observations of cultures of RAW 264.7 cells, which originated from a tumor in a Balb/c mouse that had been induced by the Abelson murine leukemia virus. RAW 264.7 cells were treated with either Ni, N- onomethyl-L- arginine (NMLA), catalase, and DTT for 24-72 h. The cytotoxicity of the nickel was measured via the cell viability and NO2-, H2O2, GSH, and the mitochondrial function was evaluated by the adenosine triphosphate (ATP) production in the RAW 264.7 cells.
RESULTS
The NO2- synthesis of RAW 264.7 cells increased with the increase in concentrations of Ni up to 50-micrometer, after 24 and 48 h of exposure, but then decreased at concentrations greater than 50-micrometer, and with time periods exceeding 48 h. In contrast, viability of cells and intracellular GSH level decreased in the presence of Ni in a dose and time dependent manner. However, the H2O2 synthesis of RAW 264.7 cells was not changed in the all experimental conditions. The NO2- synthesis of the cells was higher than control, whereas ATP, GSH and viability were lower than control in addition of Ni and the pretreatment of catalase or DTT prior to addition of Ni.
CONCLUSIONS
These results suggest that NO plays an important role in the cytotoxicity of Ni. Cytotoxicity of Ni may exert through modulation of NO production and associate with a decrease in intracellular GSH levels.

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Effect of Glutathione on Apoptosis Induced by Methyl Mercury Chloride: Jung Ho Youm, Dai Ha Koh, Keun Sang Kwon, Me Yae Lee; Korean Journal of Occupational and Environmental Medicine 2002;14(4):377-391. Published online December 31, 2002; DOI: https://doi.org/10.35371/kjoem.2002.14.4.377

Abstract PDF: 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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Cadmium-induced Apoptosis in HL-60 Cells Via Signal Transduction: Nam Song Kim, Gyung Jae Oh, Kwang Ho Cho, Mee Sun Hyun, Yoo Chang Kim, Tae Ho Sung, Jung Ho Youm, Keun Sang Kwon; Korean Journal of Occupational and Environmental Medicine 2002;14(1):1-12. Published online March 31, 2002; DOI: https://doi.org/10.35371/kjoem.2002.14.1.1

Abstract PDF

OBJECTIVES
Apoptosis is a process of active cell death, distinct from necrosis and characterized by specific morphological and biochemical features. Apoptosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metals are well described, little is known about the mechanism of apoptosis via cadmium toxicity. Therefore, this study is designed to define the induction mechanism of apoptosis by which cadmium exerts its cytotoxic effect on human promyelocytic leukemic HL-60 cells. The cytotoxic effects of cadmium on HL-60 cells are studied in regards to apoptotic signal transduction pathways.
METHODS
The mode of cadmium-induced apoptosis was investigated in HL-60 cells. HL-60 cells were treated with various concentrations of cadmium and antioxidants after which the viability of the cells were measured by MTT assay. The morphological features of cadmium- induced apoptosis were evaluated by fluoromicroscopy and the DNA fragmentation was analyzed using 1.5% agarose gel electrophorosis. Kinase activity was assayed by autoradiography and activity of NF-kappaB and nuclear proteins were measured by EMSA.
RESULTS
Cadmium (125 microM) induces the characteristic morphological features of apoptosis, which are characterized by a shrinkage of the cytoplasm and a condensation of chromatin. In addition, cadmium induced the ladder pattern of DNA fragmentation. Antioxidants(Sodium nitroprusside, glutathione and N-acethylcysteine), which were not toxic to the cells, did not suppress apoptosis induced by cadmium. Cadmium enhances the expression of several classes of genes at elevated cytotoxic concentrations. Poly(ADP-ribose) polymerase(PARP) was predominantly in the fragmented form when doses of 125 microM were used. Since PARP is cleaved by CPP32 (caspase-3), we next determined if cadmium was capable of effecting changes in CPP32 activity. The results of these experiments showed that cadmium increased caspase-3 activity in a time dependent manner, corresponding to the time of appearance of fragmented PARP. Cadmium also increased the phosphotransferase activities of c-JUN N-terminal kinase (JNK). Furthermore, cadmium increased the activation of transcriptional factors including the activation of protein-1 (AP-1) and NF-kappaB .
CONCLUSIONS
These results suggest that cadmium induces the apoptotic death of HL-60 cells via the activation of a DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kappaB .

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The association between blood cadmium level, frequency and amount of gejang (marinated crab) intake
Chang Yul Choi, Gun Il Park, Young Seok Byun, Man Joong Jeon, Kwang Hae Choi, Joon Sakong
Annals of Occupational and Environmental Medicine.2016;[Epub] CrossRef

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