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UVB exposure at ambient outdoor levels triggers rapid K+loss and apoptosis in human corneal limbal epithelial (HCLE) cells cultured in medium containing 5.5 mM K+, but considerably less apoptosis occurs when the medium contains the high K+concentration that is present in tears (25 mM). Since Ba2+blocks several K+channels, we tested whether Ba2+-sensitive K+channels are responsible for some or all of the UVB-activated K+loss and subsequent activation of the caspase cascade and apoptosis. Corneal epithelial cells in culture were exposed to UVB at 80 or 150 mJ/cm2. Patch-clamp recording was used to measure UVB-induced K+currents. Caspase-activity and TUNEL assays were performed on HCLE cells exposed to UVB followed by incubation in the presence or absence of Ba2+. K+currents were activated in HCLE cells following UVB-exposure. These currents were reversibly blocked by 5 mM Ba2+. When HCLE cells were incubated with 5 mM Ba2+after exposure to UVB, activation of caspases-9, -8, and -3 and DNA fragmentation were significantly decreased. The data confirm that UVB-induced K+current activation and loss of intracellular K+leads to activation of the caspase cascade and apoptosis. Extracellular Ba2+inhibits UVB-induced apoptosis by preventing loss of intracellular K+when K+channels are activated. Ba2+therefore has effects similar to elevated extracellular K+in protecting HCLE cells from UVB-induced apoptosis. This supports our overall hypothesis that elevated K+in tears contributes to protection of the corneal epithelium from adverse effects of ambient outdoor UVB.

Discusses issues leading to atheistic conclusions from the facts and theory of evolution. Reasons why people believe in a Creator; Assertion of the rationality and assurance of such beliefs; Versions of creationism; Implication of problems between creationism and evolution on public schools.