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.
- cell death
- corneal stroma
- corneal epithelium
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Funding FEMH-910014, Taipei, Taiwan.
Competing interests None declared.
Patient consent Obtained.
Ethics approval This study was conducted with the approval of the Institutional Review Board of the Far Eastern Memorial Hospital.
Provenance and peer review Not commissioned; externally peer reviewed.