We examined the influence of short-term exposures of different UV wavebands on the elongation and phototropic curvature of hypocotyls of cucumbers (Cucumis sativus L.) grown in white light (WL) and dim red light (DRL). We evaluated (1) whether different wavebands within the ultraviolet B (UV-B) region elicit different responses; (2) the hypocotyl elongation response elicited by ultraviolet C (UV-C); (3) whether irradiation with blue light-enriched white light (B/WL) given simultaneous with UV-B treatments reversed the effect of UV in a manner indicative of photoreactivation; and (4) whether responses in WL-grown plants were similar to those grown in DRL. Responses to brief (1-100 min) irradiations with three different UV wavebands all induced inhibition of elongation measured after 24 h. When WL-grown seedlings were irradiated with light containing proportionally greater short wavelength UV-B (37% of UV-B between 280 and 300 nm), inhibition of hypocotyl elongation was induced at a threshold of 0.5 kJ m(-2), whereas exposure to UV-B including only wavelengths longer than 290 nm (and only 8% of UV-B between 290 and 300 nm) induced inhibition of hypocotyl elongation at a threshold of 1.6 kJ m(-2). The UV-C treatment induced reduction in elongation at a threshold of <0.01 kJ m(-2) for DRL-grown plants and <0.03 kJ m(-2) for WL-grown plants. B/WL caused 50% reversal of the short-wavelength UV-B-induced inhibition of elongation in DRL-grown seedlings but did not reverse the effect of long-wavelength UV-B. B/WL caused 30% reversal of the UV-C-induced inhibition of elongation in WL-grown seedlings but did not affect the response to short-wavelength UV-B. Short-wavelength UV-B also induced positive phototropic curvature in both types of seedlings, and this was reversed 60% or completely in DRL-grown and WL-grown seedlings, respectively. The similarity of responses between the etiolated (DRL-grown) and de-etiolated (WL-grown) seedlings indicates that the short-wavelength specific response may be relevant to natural light environments, and the apparent photoreactivation implicates DNA damage as the sensory mechanism for the response.

Oxidative stress has been linked to many disease processes, including ischemia‐reperfusion injury and toxicant damage. Loss of barrier function in renal epithelial cells due to alterations in the tight junction (TJ) may complicate the effects of oxidative stress. The mitogen‐activated protein kinase (MAPK) pathway has been shown to be an early cellular signal during hydrogen peroxide exposure oxidant injury and may be linked to TJ protein alterations. In this study, we are interested in effects on cell barrier function due to a brief exposure to hydrogen peroxide and the ensuing recovery period. Transepithelial electrical resistance and paracellular flux were used as a measure of barrier integrity, while the lactate dehydrogenase activity assay was used to assess cytotoxicity. Protein expression was determined via Western blot analysis, and immunofluorescent staining was used for localization of TJ proteins and examination of the actin cytoskeleton. A positive relationship between dose of hydrogen peroxide and cytotoxicity was observed. Low doses of hydrogen peroxide perturb TJ function without exhibiting a cytotoxic effect. ERK‐1/2, an enzyme of the MAPK pathway, was activated within minutes of exposure to hydrogen peroxide as determined by phospho‐ERK content. Exposure to hydrogen peroxide with subsequent recovery was also associated with changes in expression and localization of the TJ proteins occludin and claudin‐1. These findings demonstrate that the TJ in MDCK cells is altered by exposure to hydrogen peroxide and these changes are preceded by activation of the MAPK pathway.