Cadmium (Cd) is an environmental contaminant that poses serious risks to human and wildlife health. The oxidative stress and inflammatory responses induced by Cd were evaluated in RAW264.7 cells. A significant decrease in the cell viability was observed in the group treated with 3 µM Cd for 24 h. The mRNA levels of tumor necrosis factor-α (TNFα), interleukin-6 (IL6), interleukin-1α (IL1α) and Interleukin-1β (IL1β) were generally increased or decreased by Cd exposure for 6 and 24 h, respectively. Moreover, pretreatment of the RAW264.7 cells with Cd for 24 h inhibited the transcriptional status of TNFα, IL6, IL1α and IL1β and the release of these cytokines in response to a 6-h lipopolysaccharide (LPS) treatment in a dose-dependent manner. Furthermore, the Cd exposure elicited oxidative stress not only by disturbing the transcriptional status of genes including superoxide dismutase (Sod), catalase (Cat), glutathione peroxidase(Gpx), glutathione S-transferase 1 a (Gst1a),
Nad(p)h: quinone oxidoreductase 1(Nqo1), heme oxygenase 1(Ho-1) but also the enzyme activities of SOD, CAT and glutathione S-transferase (GST). The effects of Cd on the mRNA levels and activities of anti-oxidative enzymes were dependent on the exposure period and dose. These results suggested that Cd exposure generated oxidative stress and decreased the inflammatory responses in a murine macrophage cell line. Furthermore, oxidative stress may be a possible mechanism to explain the dysregulation of the immune function caused by heavy metals in this in vitro system.
Keywords: Cadmium; Inflammatory response; Macrophage; Oxidative stress.
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