Mechanism of taxane neurotoxicity.
Mechanism of taxane neurotoxicity.
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DOI：
10.1007/bf02968008
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发表时间：
2004-01-01
期刊：
影响因子：
--
通讯作者：
Sunada, Yoshihide
中科院分区：
文献类型：
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作者：
Hagiwara, Hiroki;Sunada, Yoshihide
两种紫杉烷（紫杉醇和多西紫杉醇）广泛应用于标准抗肿瘤实践中。尽管这些药物现在已经很成熟，但也有一些毒副作用的报道。这些药物的毒性包括骨髓抑制（主要是中性粒细胞减少症）、过敏反应、皮肤反应、水肿和神经毒性。最突出的神经毒性是感觉神经病。控制神经病变对于维持患者的生活质量至关重要，因为它通常是持续性的且难以控制。紫杉烷引起的神经病变的确切机制仍不清楚。已知紫杉烷类可促进细胞内微管的聚集。神经元细胞中微管的异常聚集可能导致这种神经病。此外，紫杉烷类化合物被认为具有内在毒性并直接损伤细胞。更好地了解这种神经病变的机制可能会改善接受紫杉烷类抗肿瘤治疗的患者的生活质量。
The two taxanes (paclitaxel and docetaxel) are widely employed in standard antineoplastic practice. Although these agents are now well established, some toxic side effects have been reported. Toxicity of these agents includes bone marrow suppression (principally neutropenia), hypersensitivity reactions, cutaneous reactions, edema and neurotoxicity. The most prominent neurotoxicity is a sensory neuropathy. Controlling neuropathy is crucial for maintaining the quality of life of patients because it is usually persistent and hard to manage. The precise mechanism for taxane-induced neuropathy is still unknown. The taxanes are known to promote aggregation of intracellular microtubules. Abnormal aggregation of microtubules in the neuronal cells may cause this neuropathy. In addition, the taxanes have been suggested to have intrinsic toxicity and directly injure the cells. A better understanding of the mechanism for this neuropathy may improve the quality of life of patients who undergo taxane antineoplastic therapy.