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The effect of beta-cyclodextrin and hydroxypropyl beta-cyclodextrin incorporation into plasticised poly(vinyl chloride) on its compatibility with human monocytes

George, Susan M. and Gaylor, John D.S. and Leadbitter, Jason and Grant, M.Helen (2011) The effect of beta-cyclodextrin and hydroxypropyl beta-cyclodextrin incorporation into plasticised poly(vinyl chloride) on its compatibility with human monocytes. Journal of Biomedical Materials Research Part B: Applied Biomaterials, 96B (2). pp. 310-315.

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Abstract

Di (2-ethyl hexyl) phthalate (DEHP) is one of the main plasticizers used in poly(vinyl chloride) (PVC) medical devices and is currently the only one listed for use in the European Pharmacopoeia Monograph. It leaches out of PVC when the material is in contact with lipophilic media, for example, blood and certain nutritional feeds. Consequently, concerns have been expressed since in certain animal species, DEHP has been shown to exhibit both carcinogenic and reproductive toxic effects. Incorporation of beta cyclodextrin (BCD) and hydroxypropyl betacyclodectrin (HPBCD) into plasticized materials has been reported to decrease the leaching of DEHP. We have investigated whether this results in improved in vitro biocompatibility by measuring the responses of U937 cells to plasticized PVC in the presence and absence of added BCD or HPBCD. Growth and viability of the U937 cells, as well as tumor necrosis factor- (TNF-) production in contact with these materials revealed no significant difference between unmodified plasticized PVC materials and those containing BCD or HPBCD. Lipopolysaccharide (LPS) was used to elicit TNF- production, and the response of cells to LPS in the presence of the PVC materials was evaluated. When PVC was modified by addition of HPBCD there was a significant reduction in the TNF- production in response to LPS. Modification of plasticized PVC biomaterials by adding cyclodextrins did not significantly improve their biocompatibility. However, the HPBCD modified plasticized PVC materials caused a reduction in the production in TNF- induced by LPS which may have implications for the inflammatory potential of these biomaterials.