Sokol-Anderson M L, Brajtburg J, Medoff G
J Infect Dis. 1986 Jul;154(1):76-83. doi: 10.1093/infdis/154.1.76.
Amphotericin B (AmB) is known to bind to ergosterol in fungal cell membranes, but the precise mechanism of its toxicity to cells is as yet poorly understood. AmB autooxidizes, and it is possible that its antifungal effects could result from oxidative damage. Exposure of protoplasts of Candida albicans to AmB under hypoxic conditions reduced protoplast lysis by as much as 80% compared with incubations in air. Protoplasts were protected from AmB-induced lysis by exogenous catalase and/or superoxide dismutase (SOD). Whole cells of C. albicans were protected by exogenous catalase from AmB-induced leakage of [3H]leucine and from killing by AmB. Cells grown on medium inducing high levels of endogenous catalase were resistant to AmB-induced growth inhibition. In contrast, AmB-induced K+ leakage was not hindered under hypoxic conditions or in the presence of catalase or SOD. Thus the lethal and lytic effects of AmB on C. albicans cells and protoplasts, but not prelethal AmB-induced K+ leakage, are mediated by oxidative damage.
两性霉素B（AmB）已知可与真菌细胞膜中的麦角固醇结合，但其对细胞毒性的确切机制目前仍知之甚少。AmB会自动氧化，其抗真菌作用可能源于氧化损伤。与在空气中培养相比，在缺氧条件下将白色念珠菌原生质体暴露于AmB可使原生质体裂解减少多达80%。外源性过氧化氢酶和/或超氧化物歧化酶（SOD）可保护原生质体免受AmB诱导的裂解。外源性过氧化氢酶可保护白色念珠菌全细胞免受AmB诱导的[3H]亮氨酸泄漏以及AmB的杀伤作用。在诱导高水平内源性过氧化氢酶的培养基上生长的细胞对AmB诱导的生长抑制具有抗性。相比之下，在缺氧条件下或存在过氧化氢酶或SOD时，AmB诱导的K+泄漏并未受到阻碍。因此，AmB对白色念珠菌细胞和原生质体的致死和裂解作用是由氧化损伤介导的，但致死前AmB诱导的K+泄漏并非如此。
