Medical School, Federal University of Ceará.
Braz J Otorhinolaryngol. 2009 Sep-Oct;75(5):745-52. doi: 10.1016/S1808-8694(15)30528-0.
Cisplatin is a chemotherapy agent frequently used to treat different types of neoplasia. Ototoxicity is one of the side-effects which cause significant morbidity and limits its use. This study aimed at assessing the role of apoptosis in cisplatin-induced ototoxicity.
experimental study.
male Wistar rats were treated with intraperitoneal cisplatin, in the doses of 24 and 16 mg/kg. The animals were assessed by means of distortion product evoked otoacoustic emissions (DPEOAE) or brainstem evoked auditory potentials (BEAP) in the third (D3) and fourth (D4) days after drug infusion onset. Following that, their cochleas were removed for immunohistochemical studies of apoptosis - TUNEL method.
the group treated with 24 mg/kg showed a significant reduction in DPEOAE amplitude, and such fact was not seen with the 16 mg/kg. Both doses caused an increase in BEAP electrophysiological threshold in D3 and D4. Apoptosis was the injury mechanism responsible for the cisplatin-induced ototoxicity - 16 mg/kg dose, when the animals were assessed on D3.
apoptosis may be involved in the cisplatin-induced ototoxicity, depending on the dose and time of injury assessment.
顺铂是一种常用于治疗多种肿瘤的化疗药物。耳毒性是其引起显著发病率并限制其使用的副作用之一。本研究旨在评估细胞凋亡在顺铂诱导的耳毒性中的作用。
实验研究。
雄性 Wistar 大鼠腹腔内给予顺铂,剂量分别为 24 和 16mg/kg。在药物输注开始后的第 3(D3)和第 4(D4)天,通过畸变产物耳声发射(DPOAE)或脑干听觉诱发电位(BAEP)评估动物。随后,取出耳蜗进行细胞凋亡的免疫组织化学研究 - TUNEL 法。
24mg/kg 组 DPOAE 幅度显著降低,而 16mg/kg 组未见此现象。两种剂量均导致 D3 和 D4 时 BAEP 电生理阈值升高。细胞凋亡是顺铂诱导耳毒性的损伤机制 - 在 D3 时评估动物时,16mg/kg 剂量下。
细胞凋亡可能参与顺铂诱导的耳毒性,取决于损伤评估的剂量和时间。