Rs. Labow et al., THE EFFECT OF PHOSPHOLIPIDS ON THE BIODEGRADATION OF POLYURETHANES BYLYSOSOMAL-ENZYMES, Journal of biomaterials science. Polymer ed., 8(10), 1997, pp. 779-795
Although biodegradation of model poly(ester-urethane)s and poly(ether-
urethane)s has been demonstrated using a single enzyme system (cholest
erol esterase (CE)) in vitro, in vivo biodegradation most likely invol
ves many processes acting together. In this study, the physical (film
vs textured surface) and chemical (poly(urethane)s containing polycapr
olactone (PCL) vs poly(tetramethylene oxide) (PTMO)) nature of the mat
erials as well as the products of enzymatic reactions known to occur d
uring the inflammatory response (CE and phospholipase A(2) (PLA)) were
assessed for their effects on poly(urethane) (PU) biodegradation in v
itro. A mixed micelle (phosphatidylcholine (PC):lysoPC (LPC):oleic aci
d (OA); 2: 1 : 1) significantly increased the release of radiolabelled
products from a C-14-labelled poly(ester-urethane) (TDI/PCL/ED) cause
d by CE. This effect was further enhanced when this material was cast
as a textured surface. A model poly(ether-urethane) showed no signific
ant enhancement of CE-mediated hydrolysis in the presence of phospholi
pids and their breakdown products whether cast as a film or a textured
surface. PLA caused a small but significant release of radiolabel fro
m TDI/PCL/ED which was enhanced in the presence of its substrate, PC,
and a mixture of PC with its breakdown products, LPC and OA. Based on
the results of this study, it may be possible to hypothesize that duri
ng the inflammatory response when PLA is activated, enhancement of the
biodegradation of a PU could occur by direct action of PLA on the pol
y(ester-urethane) and by stimulation of CE due to the formation of LPC
and OA occuring when PLA hydrolyses PC, its natural substrate.