Cortopassi G, Hutchin T
Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, Los Angeles 90033.
Hear Res. 1994 Jul;78(1):27-30. doi: 10.1016/0378-5955(94)90040-x.
The ototoxic effects of aminoglycoside antibiotics are well known. However, a molecular and cellular mechanism for the death of cochlear hair cells has remained difficult to prove. Human genetic studies have shown that a rare trait for hypersensitivity to aminoglycosides is conferred by mitochondrial genetic variation. Recently, a gene involved has been identified as the mitochondrial small ribosomal RNA gene, consistent with the known mechanism of aminoglycoside action against bacteria. We used the existing data as a basis for our hypothesis of a molecular and cellular model for aminoglycoside ototoxicity that is described in this paper.
氨基糖苷类抗生素的耳毒性作用是众所周知的。然而，耳蜗毛细胞死亡的分子和细胞机制仍难以证实。人类遗传学研究表明，线粒体遗传变异赋予了对氨基糖苷类药物超敏反应的罕见性状。最近，一个相关基因已被确定为线粒体小核糖体RNA基因，这与氨基糖苷类药物对细菌的已知作用机制一致。我们以现有数据为基础，提出了本文所述的氨基糖苷类耳毒性的分子和细胞模型假说。
