To perform various physiological functions, erythrocytes possess a unique biconcave shape provided by a special architecture of the membrane-skeleton system. In the present work, we use a simple irradiation method to treat human erythrocytes with 365 nm ultraviolet-A (UVA) light at the single-cell level in vitro. Depending on the irradiation dose, UVA show protection of the biconcave profile against the detrimental action of distilled water. This protective effect can also be confirmed for saponin that damages the membrane-skeleton by vesiculation and pore formation. Interestingly, at two irradiation doses of UVA pretreatment, erythrocytes still seem to exhibit cell viability as tested by trypan blue assay even if distilled water or saponin is added. The oxidants hydrogen peroxide and cumene hydroperoxide partly simulate the protective effects. Taken together, these results demonstrate that 365 nm UVA irradiation can protect the biconcave profile of human erythrocytes through membrane-skeleton enhancement associated with a production of oxidants.

Ultraviolet blood irradiation has been used as a physical therapy to treat many nonspeci¯c diseases in clinics; however, the underlying mechanisms remain largely unclear. Neutrophils, thē rst line of host defense, play a crucial role in a variety of in°ammatory responses. In the present work, we investigated the e®ects of ultraviolet light A (UVA) on the immune functions of human neutrophils at the single-cell level by using an inverted°uorescence microscope. N-Formylmethionyl-leucyl-phenylalanine (FMLP), a classic physiological chemotactic peptide, was used to induce a series of immune responses in neutrophils in vitro. FMLP-induced calcium mobilization, migration, and phagocytosis in human neutrophils was signi¯cantly blocked after treatment with 365 nm UVA irradiation, demonstrating the immunosuppressive e®ects of UVA irradiation on neutrophils. Similar responses were also observed when the cells were pretreated with H 2 O 2 , a type of reactive oxygen species (ROS). Furthermore, UVA irradiation resulted in an increase in NAD(P)H, a member of host oxidative stress in cells. Taken together, our data indicate that