1. Modulation of intercellular communication mediated at the cell surface and on extracellular, plasma membrane–derived vesicles by ionizing radiation 
Joseph Albanese, Nicholas Dainiak 
Experimental Hematology 
Volume 31, Issue 6, Pages (June 2003)
DOI: /S X(03)00050-X

2. Figure 1
Plasma membrane damage results from lipid peroxidation. Lipid peroxidation is initiated by a hydroxyl radical, which abstracts a hydrogen atom from polyunsaturated lipid molecules (lipid). This generates a lipid radical, where electron shuffling leads to the formation of conjugated lipid radicals. Molecular oxygen adds to the conjugated lipid radical to form a lipid peroxyl which, in turn, abstracts a hydrogen atom from a nearby lipid molecule to produce a lipid hydroperoxide molecule, while regenerating the lipid radical. This lipid radical can react with another lipid molecule and begin the cycle again. Hence the hydroxyl radical initiates a reaction which is self-perpetuating and results in the oxidative deterioration of polyunsaturated lipid molecules [12].
Experimental Hematology  , DOI: ( /S X(03)00050-X)

3. Figure 2
Biophysical alterations of the plasma membrane induced by IR. (See text for details.)
Experimental Hematology  , DOI: ( /S X(03)00050-X)

4. Figure 3
SVs collected from lymphocytes and examined under freeze-fracture electron microscopy. Vesicles in panel A exhibit protrusions that are believed to be integral proteins. In contrast, SVs in panel B are smooth, indicating an absence of transmembrane proteins. Transmission electron microscopy reveals that SVs lack cytoplasmic organelle. Reproduced with permission [50,58].
Experimental Hematology  , DOI: ( /S X(03)00050-X)

5. Figure 4
Cumulative shedding from irradiated (0.5 Gy) and nonirradiated (control) T lymphocytes. Cells exposed to IR shed significantly less protein in association with SVs, relative to control cells.
Experimental Hematology  , DOI: ( /S X(03)00050-X)

6. Figure 5
TNFSF6-bearing SVs (alone) induce cell death in TNFSF6-sensitive Jurkat cells. Pretreatment with anti-TNFSF6 antibody (Anti-FasL Ab) partially inhibits SV-mediated apoptosis. Jurkat cells treated with CHO SVs or Anti-TNFRSF6 antibody (Anti-Fas) served as negative and positive controls, respectively. Reproduced with permission [42].
Experimental Hematology  , DOI: ( /S X(03)00050-X)

7. Figure 6
T lymphocytes treated with staurosporine (A), a PKC inhibitor, show a significant reduction in rate of shedding, compared to untreated (control) cells. In contrast, PMA (B), a PKC activator, increases the rate of shedding in lymphocytes.
Experimental Hematology  , DOI: ( /S X(03)00050-X)

8. Figure 7
Irradiated colon cancer cells (SW620) exhibit a dose-dependent increase in TNFSF6 mRNA transcription. Reproduced with permission [42].
Experimental Hematology  , DOI: ( /S X(03)00050-X)

9. Figure 8
Colon cancer cells (SW620) treated with IR (4 and 10 Gy) release SVs with significantly less apoptotic activity, relative to nonirradiated cells (0 Gy). SVs from CHO cells and anti-TNFRSF6 antibody (Anti-Fas) served as negative and positive controls, respectively. Reproduced with permission [42].
Experimental Hematology  , DOI: ( /S X(03)00050-X)