ABSTRACT
In haemodialysis patients, increased concentrations of malonyldialdehyde and decreased vitamin E content indicate lipid peroxidation in the platelets from oxidative damage. The same process has been described in red blood cells and in mononuclear cells in peripheral blood. However, platelet aggregation is within normal limits and does not change after treatment with vitamin E. On the other hand vitamin E supplementation reverts completely the biochemical abnormality of the platelets.
Subject(s)
Blood Platelets/metabolism , Kidney Failure, Chronic/therapy , Lipid Peroxidation/drug effects , Renal Dialysis , Vitamin E/therapeutic use , Female , Humans , Kidney Failure, Chronic/blood , Male , Malondialdehyde/blood , Middle Aged , Vitamin E/bloodABSTRACT
Several reports have appeared showing the possibility of bilirubin-sensitized photodamage. We have extended these observations to platelets. In the presence of 300 microM bilirubin the in vitro irradiation of isolated platelets or platelet-rich plasmas with visible light induced significant lysis as determined by the release of lactate dehydrogenase (LDH). The extent of LDH release was a function of irradiation time, being about 20% after 2 h of irradiation. A loss membrane-bound ATPase activity was also observed at earlier times, indicating that membrane damage was preliminary to the lytic effect. The release of beta-thromboglobulin, induced by close cell-to-cell contact, was lower in bilirubin- and light-treated platelets with respect to controls. Our results suggest that bilirubin may act as a photodynamic agent producing some damage on human blood platelets.