To gain an understanding of the toxicity of antimicrobial polymers to human cells, their hemolytic action was investigated using human red blood cells （RBCs）. We examined the hemolysis induced by cationic amphiphili...To gain an understanding of the toxicity of antimicrobial polymers to human cells, their hemolytic action was investigated using human red blood cells （RBCs）. We examined the hemolysis induced by cationic amphiphilic methacrylate random copolymers, which have amino ethyl sidechains as cationic units and either butyl or methyl methacpjlate as hydrophobic units. The polymer with 30 tool% butyl sidechains （B3o） displayed higher hemolytic toxicity than the polymer with 59 tool% methyl sidechains （Ms9）. B3o also induced faster release of hemoglobin from RBCs than lVlsg. A new theoretical model is proposed based on two consecutive steps to form active polymer species on the RBC membranes, which are associated to RBC lysis. This model takes the all-or-none release of hemoglobin by the rupture of RBCs into account, providing new insight into the polymer-induced hemolysis regarding how individual or collective ceils respond to the polymers.展开更多
基金supported by the Department of Biologic and Materials Sciences,University of Michigan School of Dentistry,NSF CAREER Award (No.DMR-0845592 to KK)JSPS KAKENHI,Grant-in-Aids for Challenging Exploratory Research (No.25650053)Young Scientists (Nos.24681028 and 22700494 to KY)
文摘To gain an understanding of the toxicity of antimicrobial polymers to human cells, their hemolytic action was investigated using human red blood cells （RBCs）. We examined the hemolysis induced by cationic amphiphilic methacrylate random copolymers, which have amino ethyl sidechains as cationic units and either butyl or methyl methacpjlate as hydrophobic units. The polymer with 30 tool% butyl sidechains （B3o） displayed higher hemolytic toxicity than the polymer with 59 tool% methyl sidechains （Ms9）. B3o also induced faster release of hemoglobin from RBCs than lVlsg. A new theoretical model is proposed based on two consecutive steps to form active polymer species on the RBC membranes, which are associated to RBC lysis. This model takes the all-or-none release of hemoglobin by the rupture of RBCs into account, providing new insight into the polymer-induced hemolysis regarding how individual or collective ceils respond to the polymers.
