BACKGROUND: B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) is a Bcl-2 family member with sequence homology to pro-apoptotic BAX and BAK, but its physiological and pathological roles remain largely unclear. Exposure of cells to cadmium may cause DNA damage, decrease DNA repair capacity, and increase genomic instability.

MATERIAL AND METHODS: The present study investigated the effects of BOK on the toxicity of cadmium chloride (CdCl₂) to human bronchial epithelial (16HBE) cells. We constructed BOK over-expressing (16HBE-BOK) cells and BOK knockdown (16HBE-shBOK) cells using the BOK-ORF plasmid and BOK-siRNA. qRT-PCR for BOK mRNA expression. We used Trypan blue exclusion assay for cell growth, MTT colorimetric assays for cells inhibition rate, and Comet assays for detecting damaged DNA.

RESULTS: CdCl₂, at various concentrations and exposure times, increased BOK mRNA. 16HBE-BOK cells (BOK over-expressing) proliferated more than 16HBE cells after 72 h; 16HBE-shBOK (BOK knockdown) cells proliferated less. In addition, BOK deficiency enhanced cell death induced by CdCl₂. Similarly, CdCl₂- and H₂O₂-induced DNA damage was greater in BOK-deficient cells.

CONCLUSIONS: These findings support a role for BOK in CdCl₂-induced DNA damage and cell death.

Keywords: bcl-Associated Death Protein, Cadmium Chloride, Comet Assay, Bronchi, Cell Cycle, Cell Death, Cell Line, DNA Damage, Lung, Proto-Oncogene Proteins c-bcl-2, RNA, Messenger