Background/aims: Povidone-iodine (PI) is commonly used as a preoperative disinfectant; however, it has been shown to be cytotoxic. The present study was performed to investigate the mechanism by which PI causes cell death.
Methods: Primary human corneal fibroblasts (HCF) and a human corneal epithelial cell line (HCEC) were treated with 0.1-5% PI for 1 min. Cell morphology and growth were examined by phase-contrast microscopy and genomic DNA quantification. Cellular enzyme activities were detected by water-soluble tetrazolium salt (WST-1) and calcein-acetoxymethylester staining, whereas membrane integrity was determined by a membrane-impermeable dye. The cell fixation effect of PI was assayed by analysis of genomic DNA integrity and resistance to ionic detergent SDS lysis. The interleukin-8 (IL-8) secretion after adding interleukin-1ß (IL-1b) or lipopolysaccharide (LPS) was determined by ELISA.
Results: PI treatment inhibited HCF and HCEC cell growth without changing cellular morphology; however, cells became resistant to SDS lysis. The mitochondrial dehydrogenase and intracellular esterase activities as well as cell membrane integrity were abolished by PI treatment. Genomic DNA integrity from PI-treated groups was similar to that from alcohol-fixed groups. IL-1b- and LPS-induced IL-8 secretion was abolished by PI treatment.
Conclusions: Where PI concentration is sufficient to cause cell death, this occurs through fixation rather than necrosis in cultured human corneal stromal and epithelial cell.