Effects of cadmium chloride on the cultured human lens epithelial cells.

PURPOSE: To investigate cadmium chloride cytotoxicity in human lens epithelial cells as well as the mode of cell death and its mechanism. METHODS: Cultured human lens epithelial cells were challenged with cadmium chloride. Morphological changes of human lens epithelial cells caused by cadmium chloride exposure were evaluated by microscope. Cell viability was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-dipheny tetrazolium bromice (MTT) assay. To explore the mechanism of cell death, p53 and caspase-8 levels were measured by western blotting. RESULTS: Microscopic examination indicated that cell death increased after cadmium chloride exposure compared to untreated cells. The MTT assay demonstrated that cadmium chloride significantly decreased cell viability in a dose dependent way. Western blot and quantitative analysis showed that both p53 and caspase-8 increased after cell exposure to cadmium chloride. p53 increased 210% and caspase-8 increased 30% in the experimental group as compared with the control group. CONCLUSIONS: Cadmium chloride induced cytotoxicity and apoptosis in human lens epithelial cells and the mechanism of apoptosis involve an increased expression of p53 and caspase-8.

Achromobacter xylosoxidans keratitis after contact lens usage.

To report on Achromobacter xylosoxidans keratitis in two healthy patients who had worn contact lenses foran extended period of time. A 36-year-old female and a 21-year-old female visited our hospital with ocular pain and blurred vision. Both patients had a history of wearing soft contact lenses for over fve years with occasional overnight wear. At the initial presentation, a slit lamp examination revealed corneal stromal infiltrations and epithelial defects with peripheral neovascularization in both patients. Microbiological examinations were performed from samples of corneal scrapings, contact lenses, contact lens cases, and solution. The culture resulting from the samples taken from the contact lenses, contact lens cases, and solution were all positive for Achromobacter xylosoxidans. Confrming that the direct cause of the keratitis was the contact lenses, the frst patient was prescribed ceftazidime and amikacin drops sensitive to Achromobacter xylosoxidans. The second patient was treated with 0.3% gatifoxacin and fortifed tobramycin drops. After treatment, the corneal epithelial defects were completely healed, and subepithelial corneal opacity was observed. Two cases of Achromobacter xylosoxidans keratitis were reported in healthy young females who wore soft contact lenses. Achromobacter xylosoxidans should be considered a rare but potentially harmful pathogen for lens-induced keratitis in healthy hosts.