Annals of Occupational and Environmental Medicine

Original Article

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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Original Article

Autoregulation of Quartz-induced iNOS by iNOS-derived Hydrogen Peroxide in Rat2 Fibroblast: Kyoung Ah Kim, Hae Yun Nam, Je Hyeok Mun, Jin Sook Jeong, Young Lim, Chee Kyung Chung; Korean Journal of Occupational and Environmental Medicine 2001;13(4):385-392. Published online December 31, 2001; DOI: https://doi.org/10.35371/kjoem.2001.13.4.385

Abstract PDF: OBJECTIVES
This study was performed in order to investigate the molecular mechanism regulating nitric oxide synthase(NOS) induced by alpha-quartz in Rat2 fibroblast.
METHODS
alpha-quartz-induced nitric oxide(NO) and H2O2 formation and alpha- quartz-induced iNOS protein expression in Rat2 fibroblast were monitored. With iNOS inhibitor(L-N6- (1-iminoethyl)lysine hydrochloride, L-NIL) or antioxidant(catalase), we observed NO and H2O2 formation and iNOS protein expression in Rat2 fibroblast stimulated with alpha-quartz.
RESULTS
alpha-quartz stimulated iNOS-induced NO and H2O2 formation in Rat2 fibroblast. L-NIL inhibited H2O2 formation and iNOS protein expression by alpha-quartz in Rat2 fibroblast. Pretreatment with catalase blocked the autoinhibitory pathway of iNOS by iNOSinduced H2O2, therefore H2O2 and NO production and iNOS protein expression were increased in Rat2 fibrobalst stimulated with alpha-quartz CONCLUSIONS: alpha-quartz-induced iNOS stimulated H2O2 formation in Rat2 fibroblast. INOS-induced H2O2 by alpha-quartz plays an important role in the autoinhibition pathway for regulating the iNOS function in Rat2 fibroblast

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