Membranes as targets of ultraviolet radiation

In non-photosynthetic cells, evidence for UV (ultraviolet radiation) damage to membranes comes from electron microscopy, chemical analysis and observations of transport processes. Specific perturbations in transport across membranes occur quickly after a relatively low fluence of UV. As an example, irradiation of suspension-cultured rose cells with 500-2000 J m^?2 (at 254 nm) causes an appearance of K⁺ in the extracellular medium at the rate of 5 × 10^?10μmol cell^?1 min^?1 for 30 to 60 min and more slowly thereafter. The early, rapid phase of appearance of K⁺ reflects both an increase in efflux and a decrease in influx. The appearance of K⁺ is matched by an appearance of HCO^?₃ in the medium. The HCO^?₃ comes from respiratory CO₂, which hydrates and dissociates in the cytoplasm, leading to a decrease in cytoplasmic pH. Overall, these results not only demonstrate UV damage to membrane function, but also suggest several ways by which UV may alter the general metabolic state of the cell. A demonstration of direct effects of UV on membrane components requires a purified system. At lower fluence, < 1800 J m^?2 (254 nm), the ATPase of membrane vesicle preparations is inactivated in a two-phase process that suggests the presence of enzymes with different UV sensitivities. The existence of two non-mitochondrial enzymes in rose cell vesicles has been confirmed by solubilizing the vesicle proteins with 1% cholic acid and separating the components on G-150 Sephadex. One component of relatively high molecular weight is especially sensitive. The fact that it is still sensitive when it is dissolved in cholic acid strongly suggests that its sensitivity is intrinsic and does not depend on sensitization by other membrane components. The action spectrum for the inactivation of the ATPase has a major peak at 290 nm and extends into the UV-C and UV-A regions. The physiological effects of UV-stimulated membrane changes are uncertain. There is little evidence that the UV damage to membranes is responsible for cell death. A UV-induced loss of K⁺ from guard cells may result in lower stomatal conductance. UV-stimulated membrane changes may play a role in the UV-induced synthesis of anthocyanins.