Aim:  To evaluate the ability of high‐energy ultraviolet A (UVA) light‐emitting diode (LED) to inactivate bacteria in water and investigate the inactivating mechanism of UVA irradiation. Methods and Results:  We developed a new disinfection device equipped with high‐energy UVA‐LED. Inactivation of bacteria was determined by colony‐forming assay. Vibrio parahaemolyticus, enteropathogenic Escherichia coli, Staphylococcus aureus and Escherichia coli DH5α were reduced by greater than 5‐log10 stages within 75 min at 315 J cm−2 of UVA. Salmonella enteritidis was reduced greater than 4‐log10 stages within 160 min at 672 J cm−2 of UVA. The formation of 8‐hydroxy‐2′‐deoxyguanosine in UVA‐LED irradiated bacteria was 2·6‐fold higher than that of UVC‐irradiated bacteria at the same inactivation level. Addition of mannitol, a scavenger of hydroxyl radicals (OH˙), or catalase, an enzyme scavenging hydrogen peroxide (H2O2) to bacterial suspensions significantly suppressed disinfection effect of UVA‐LED. Conclusion:  This disinfection system has enough ability to inactivate bacteria and OH˙ and H2O2 participates in the disinfection mechanism of UVA irradiation. Significance and Impact of the Study:  We newly developed UVA irradiation system and found that UVA alone was able to disinfect the water efficiently. This will become a useful disinfection system.

Ultraviolet (UV) irradiation is an effective disinfection method. In sterilization equipment, a low-pressure mercury lamp emitting an effective germicidal UVC (254 nm) is used as the light source. However, the lamp, which contains mercury, must be disposed of at the end of its lifetime or following damage due to physical shock or vibration. We investigated the suitability of an ultraviolet light-emitting diode at an output wavelength of 365 nm (UVA-LED) as a sterilization device, comparing with the other wavelength irradiation such as 254 nm (a low-pressure mercury lam) and 405 nm (LED). We used a commercially available UVA-LED that emitted light at the shortest wavelength and at the highest output energy. The new sterilization system using the UVA-LED was able to inactivate bacteria, such as Escherichia coli DH5 alpha, Enteropathogenic E. coli, Vibrio parahaemolyticus, Staphylococcus aureus, and Salmonella enterica serovar Enteritidis. The inactivations of the bacteria were dependent on the accumulation of UVA irradiation. Taking advantage of the safety and compact size of LED devices, we expect that the UVA-LED sterilization device can be developed as a new type of water sterilization device.

We showed that V. parahaemolyticus infection of Caco-2 cells results in the secretion of IL-8, and that VP1680 plays a pivotal role in manipulating host cell signaling and is responsible for triggering IL-8 secretion.

The SOS response is a global regulatory network for repairing DNA damage induced by various environmental stresses such as UV irradiation. The Escherichia coli SOS response has been extensively studied. However, there are no reports on the SOS response in Vibrio parahaemolyticus. In this study, we examined the SOS response in V. parahaemolyticus and compared the differential expression of genes induced by UVC and UVA irradiation. In UVC-exposed wild-type cells, expression of several DNA repair genes was increased. However, expression of these genes was not increased in ΔrecA or lexA mutants. Cell filamentation was observed in wild-type cells, but not in ΔrecA and lexA mutant cells. Sensitivity to UVC was significantly increased in ΔrecA, lexA mutant and Δlon strains compared with wild type. In the case of UVA irradiation, LexA-controlled DNA repair genes were minimally induced and cell filamentation was not observed. Sensitivity to UVA was the same in the mutant and wild-type strains. These findings suggest that there is a RecA-LexA-mediated SOS response in V. parahaemolyticus, and that this response is important to UVC tolerance but does not contribute to UVA tolerance.

The effects of insulin on the vasculature are significant because insulin resistance is associated with hypertension. To increase the understanding of the effects of insulin on the vasculature, we analyzed changes in potassium ion transport in cultured vascular smooth muscle cells (VSMCs). Using the potential-sensitive fluorescence dye bis-(1,3-dibutylbarbituric acid)trimethine oxonol [DiBAC₄(3)], we found that insulin induced membrane hyperpolarization after 2 min in A10 cells. Insulin-induced hyperpolarization was suppressed by glibenclamide, an ATP-sensitive potassium (K_ATP) channel blocker. Using a cell-attached patch clamp experiment, the K_ATP channel was activated by insulin in both A10 cells and isolated VSMCs from rat aortas, indicating that insulin causes membrane hyperpolarization via K_ATP channel activation. These effects were not dependent on intracellular ATP concentration, but wortmannin, a phosphatidylinositol 3-kinase (PI3-K) inhibitor, significantly suppressed insulin-induced K_ATP channel activation. In addition, insulin enhanced phosphorylation of insulin receptor, insulin receptor substrate (IRS)-1 and protein kinase B (Akt) after 2 min. These data suggest that K_ATP channel activation by insulin is mediated by PI3-K. Furthermore, using a nitric oxide synthase (NOS) inhibitor, we found that NOS might play an important role downstream of PI3-K in insulin-induced K_ATP channel activation. This study may contribute to our understanding of mechanisms of insulin resistance-associated hypertension.