Hepatic oxidative stress and inflammatory responses with cadmium exposure in male mice.

ABSTRACT

Cadmium (Cd), a non-essential heavy metal, is one of the major environmental contaminants with grave toxicological consequences globally. In the present study, the effects of Cd on hepatic oxidative stress and inflammatory responses in mice were evaluated. Male adult mice were orally exposed to 3, 10 and 30mg/L CdCl2 supplied in the drinking water for 7 and 21 days. Histopathological changes and the alterations of the main parameters related to oxidative stress and inflammatory responses in the liver were observed. Hepatic malondialdehyde (MDA) contents increased significantly after treatment with 30mg/L CdCl2 for 21 days, and the contents of glutathione (GSH) increased significantly in both 10 and 30mg/L CdCl2 treated groups. The hepatic activities of glutathione peroxidase (GPX), catalase (CAT) and glutathione S-transferase (GST) increased significantly after the treatment with 30mg/L CdCl2 for 21 days. In accordance with the enzyme activities, the transcription status of hepatic superoxide dismutase 1 (Sod1), superoxide dismutase 2 (Sod2), Cat, Gpx, Gstα1, glutathione synthetase (Gss), glutathione reductase (Gr) and heme oxygenase 1 (Ho1) were also increased by high dose (30mg/L) or long period (21 days) exposure. In addition, the serum levels of tumor necrosis factor α (TNFα), interleukin 6 (IL6) and interleukin 1ß (IL1ß) increased significantly in the groups treated with 30mg/L CdCl2 for 21 days. And the genes of TNFα, IL6, interleukin 1α (IL1α), inducible nitric oxide synthase (iNOS) and interferon γ (IFNγ) were also increased in the liver of mice when exposed to relative high dose of CdCl2 for 7 or 21 days. Taken together, the results of this study suggested that the exposure to Cd had the potential to induce immunotoxicity accompanied with oxidative stress in the liver of mice.