Alteration of protein synthesis and cell death in mouse organs under long-lasting exposure to cadmium

Objective: The present study was conducted to investigate tissue damage under prolonged oral administration of mice with cadmium chloride (CdCl2) with emphasis being placed on cadmium(Cd)-induced cell death in mice liver. Material and Methods: Juvenile (4- to 6-week-old) outbred mice were used in the experiments. Mice of the experimental group (n = 24) received drinking water supplemented with CdCl2 (250 mg elemental Cd/l) as the only drinking fluid for 8 weeks. Mice of the control group (n = 22) had free access to drinking water. All mice were terminated after 8 weeks. Protein synthesis was evaluated by incorporation of [14C]-labelled leucine into newly synthesized peptides and proteins. Apoptosis of liver cells was histochemically detected by the TUNEL assay using in situ cell death detection kit, AP (Roche, Mannheim, Germany). Results: General toxic effect of Cd was assessed according to mice body weight gain and the relative weight index of organs. In respect to the control group, the body weight gain of experimental mice was 40 – 60% lower throughout the period of Cd-administration. Small but significant increment of the relative weight index of the kidney was also revealed in Cd-affected mice. In this group, intensities of protein synthesis in liver, kidney and the heart were significantly higher than in controls. In the sections of liver specimens from Cd-affected mice, the number of TUNEL+ cells containing fragmented nuclei was significantly higher than in control (p < 0.0001); median score was 1. Conclusion: Long-term oral administration by CdCl2 activates the synthesis of proteins and induces apoptotic cell death in the liver.