Induction of cytotoxic and genotoxic damage following exposure of V79 cells to cadmium chloride

- Decreased clonogenic survival following exposure to CdCl2.
- Enhanced caspase and PARP cleavage following exposure to CdCl2.
- Increased formation of double and single strand breaks in exposed cells.
- Exposure to cadmium results in micronuclei formation and mutations at the Hprt gene.
- Induction of cytotoxic and genotoxic damage occurs a low intracellular cadmium concentrations.

Cadmium is a toxic heavy metal with many industrial and commercial uses resulting in widespread environmental pollution. Exposure to cadmium occurs occupationally, through tainted food, tobacco leaves, and the environment. Cadmium exposure has been linked to neurological and respiratory problems and cancer. Past studies have examined cytotoxicity, DNA damage, micronuclei formation, or mutagenesis individually, but no study has examined these endpoints together and correlated them with intracellular cadmium concentrations. This study examines the cytotoxic, genotoxic, and mutagenic effects of cadmium exposure in V79 cells providing a correlation between the induction of DNA damage, the generation of mutations, and intracellular cadmium concentration. Cells exposed to 2.5-40 μM cadmium exhibited a concentration-dependent decrease in survival which correlated with increases in PARP cleavage and caspase activity. Cytotoxicity was detected at intracellular cadmium concentrations of 12.9 ppb. Exposure to cadmium also resulted in the production of single and double strand breaks and the induction micronuclei and mutations in the Hprt gene. Collectively, this study demonstrates that exposure of V79 cells to cadmium results in the induction of apoptosis which is related to the formation of DNA strand breaks and genotoxic damage.