Ultraviolet A radiation (UVA) exerts a complex action on Gram negative bacteria. Within a variety of cellular components absorbing energy in this wavelength range, flavoproteins and cytochromes of the respiratory chain seem to be the chromophores involved in killing the cell. Damaged components of the respiratory chain would produce hydrogen peroxide and superoxide anion, and these compounds would generate hydroxyl radical, which is likely the main intermediary in the induction of oxidative damage. The identity of the targets remains an open question. For a long time, damage to DNA was considered to be the event leading to cell death, but recently energy depletion due to the inactivation of the respiratory chain has been proposed as an alternative mechanism. At sublethal doses UVA produces, among other effects, a transient inhibition of growth without change in viability. The growth lag is due to the inactivation of some tRNAs, which impairs protein synthesis and triggers the stringent response. A photo-protective function was ascribed to this effect. Global genetic regulators have been implicated in UVA response. The rpoS system has a strong influence on bacterial UVA resistance, probably related to the control of the response to oxidative stress, and the quorum sensing system modifies both lethal and sublethal effects of UVA in Pseudomonas. The current knowledge of the lethal action of UVA in bacteria could be improved by further analysis of the UVA response in a variety of bacterial species.