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ULTRAVIOLET RADIATION‐INDUCED PHOSPHOLIPASE A 2 ACTIVATION OCCURS IN MAMMALIAN CELL MEMBRANE PREPARATIONS
Author(s) -
Cohen Dianne,
DeLeo Vincent A.
Publication year - 1993
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1993.tb02306.x
Subject(s) - biophysics , chemistry , ultraviolet radiation , ultraviolet , membrane , cell membrane , phospholipase , cell , microbiology and biotechnology , biochemistry , enzyme , biology , radiochemistry , physics , optics
Ultraviolet erythema in human skin is mediated in part by membrane derivatives of arachidonic acid (AA). UVA (320–400nm) and UVB (290–320nm) have been shown to induce release of AA from intact mammalian cells in culture. In order to investigate the mechanism of this release we examined the effect of UVA and UVB on release of [ 3 H] AA from membrane preparations of murine fibroblasts. C3H 10T1/2 cells were prelabelled for 24 h with [ 3 H] AA. The membrane fractions of the cells were separated after lysis by differential centrifugation. The membranes were irradiated in suspension and the [ 3 H] AA released from the membranes was determined by scintillation spectroscopy of supernatants3–4 h after irradiation. Both UVA and UVB induced release of AA from the membrane preparations. The response to UVB was small but significant, reaching levels approximately 150% of control release at doses of 1,200‐4,000 J/m 2 . The response to UVA was larger; doses of 2.5‐5.0 J/cm 2 induced release equal to twice control (200%) levels, while doses of10–20 J/cm 2 induced maximal release at levels approximately 400% of control. Time course studies with UVB and UVA showed maximal release at 4 h after irradiation. When the membrane preparations were incubated with a polyclonal anti‐phospholipase A 2 antibody the UV induced release of [ 3 H] AA was completely inhibited in both UVB (1200 J/m 2 ) and UVA (10 J/cm 2 ) treated cells. These data suggest that activation of phospholipase A 2 is responsible for the UV induced release of AA in mammalian cells and that the mechanism of this activation is due, in part at least, to direct photon‐membrane interaction.