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Korean J Occup Environ Med. 1997 Jun;9(2):320-331. Korean. Original Article. https://doi.org/10.35371/kjoem.1997.9.2.320
Kang MJ , Yang SH , Chung IS , Shin DH , Park KK , Suh SK .
Department of Preventive Medicine and Public Health, School of Medicine, Keimyung University, Korea.
Department of Occupational and Environmental Medicine, Dongsan Hospital, Keimyung University, Korea.
Department of Pathology, School of Medicine, Keimyung University, Korea.
Abstract

Cadmium, a potent toxic metal, poses a serious environmental threat but the mechanism of its toxicity remains unclear. Also, cadmium is a known immunotoxic agent in animal studies and induces pathophysiological effects by modulating components of immune system. Cytokines are being increasingly recognized as essential mediators of normal and pathologic immune response. Cells of mononuclear phagocytic system are strategically located at portals of entry in humans and therefore may be particularly at risk for cadmium exposure through contaminated air, food, and drinking water. In the present study, we investigated the effect of cadmium cytotoxicity for the monocyte and expression of cytokine gene in the control and cadmium treated human monocytic cell lines using RT-PCR method. The results showed that cadmium inhibited cell proliferation at 0.1mM cadmium treated cells for 24 hours. The TNF-alpha mRNA was expressed in both control and cadmium treated cells but not IL-6 and IL-1 beta The mRNA levels of TNF-alpha were examined during 24 hours culture period, at different time points. The expression of TNF-alpha mRNA increased in both 0.01mM and 0.1mM cadmium treated cells, but did not show dose-response relationship. According to cadmium treated duration, expression of TNF-alpha mRNA was more decreases in 24 hours than 6 hours. The decreased levels of mRNA of TNF-alpha that cadmium suppresses iris production at the transcription level.

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