Oxidative mechanisms of toxicity of low-intensity near-UV light in Salmonella typhimurium

Abstract

The exposure of Salmonella typhimurium to environmentally relevant near-UV light stress has been studied by the use of a low-intensity, broad-band light source. The exposure of cells to such a light source rapidly induced a growth delay; after continuous exposure for 3 to 4 h, cells began to die at a rapid rate. The oxidative defense regulon controlled by the oxyR gene was involved in protecting cells from being killed by near-UV light. This killing may be potentiated by the overexpression of near-UV-absorbing proteins. These results are consistent with near-UV toxicity involving the absorption of light by endogenous photosensitizers, leading to the production of active oxygen species. We have shown, however, that one such species, H2O2, is not a major photoproduct involved in killing by near-UV light. Strains lacking alkyl hydroperoxide reductase were more sensitive to near-UV light, indicating that such hydroperoxides may be photoproducts. Near-UV exposure induced sensitivity to high salt levels, indicating that membranes may be a target of near-UV toxicity and a possible source of alkyl hydroperoxides. The demonstration of the inactivation of the heme-containing protein catalase indicates that direct destruction of UV-absorbing macromolecules could be another factor in near-UV toxicity. Cells which have been exposed to near-UV light for long, but sublethal, periods of time (up to 4 h) can recover and resume growth if the UV exposure is stopped but become progressively more sensitive to further stresses, such as H2O2. This result indicates that cells gradually accumulated damage during near-UV exposure until toxic levels were reached.