Protective effect of thymoquinone against cisplatin-induced ototoxicity

Abstract

The aim of this study was to investigate the potential protective effect of thymoquinone against cisplatin-induced ototoxicity. This study is a prospective, controlled experimental animal study. Experiments were performed on 30 healthy female Sprague-Dawley rats. Thirty animals were divided into three groups of 10 animals each. Group 1 received an intraperitoneal (i.p.) injection of cisplatin 15 mg/kg. Group 2 received i.p. thymoquinone 40 mg/kg/day for 2 days prior to cisplatin injection and third day i.p. cisplatin 15 mg/kg was administered concomitantly. Group 2 continued to receive i.p. thymoquinone until fifth day. Group 3 received i.p. thymoquinone 40 mg/kg/day for 5 days. Pretreatment distortion product otoacoustic emissions (DPOAE) and auditory brain stem responses (ABR) testing from both ears were obtained from the animals in all groups. After the baseline measurements, drugs were injected intraperitonally. After an observation period of 3 days, DPOAE measurements and ABR testing were obtained again and compared with the pretreatment values. There was no statistically significant difference between pre and post-treatment DPOAE responses and ABR thresholds group 2 and 3. However, group 1 demonstrated significant deterioration of the ABR thresholds and DPOAE responses. Our results suggest that DPOAE responses and ABR thresholds were preserved in the cisplatin plus TQ-treated group when compared with the group receiving cisplatin alone. According to these results, cisplatin-induced ototoxicity may be prevented by thymoquinone use in rats.

New treatment options for hearing loss

“…However, some of these may interfere with the beneficial effects of platinum drugs [179][180][181][182][183] . Moreover, none of these reagents has been tested in humans.…”

Investigation of the effects of curcumin, vitamin E and their combination in cisplatin-induced testicular apoptosis using immunohistochemical technique

“…In another study, it has been demonstrated that cisplatin may lead to production of excess amounts of free radicals, and destructive changes in DNA. [13] Apoptosis is a controlled, and programmed cell death which may become apparent under normal growth and development or as a component of a response to exposure to radiation, toxins or ischemia. Apoptosis has been asserted probably as main outcome of cisplatin-induced toxicity.…”

“…Available evidence demonstrate that increases in ROS production, and expression of endogenous antioxidant molecules support cisplatin toxicity. [11][12][13][14] As a result of OS, priorly, apoptotic cell loss occurs. [15] Cisplatin may produce reactive oxygen species, and inhibit antioxidant enzymes in normal tissues.…”

The Protective Effect of Chrysin Against Cisplatin İnduced Ototoxicity in Rats

“…Many antioxidant agents have been used to prevent cisplatin-induced ototoxicity in experimental animal or clinical trials [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][33][34][35][36][37]. Kizilay et al [5] performed an experimental study on the protective effect of caffeic acid phenethyl ester (CAPE) on cisplatin ototoxicity and reported that CAPE may have a protective effect.…”

“…Amelioration of cisplatin-induced ototoxicity has been demonstrated in studies, with many reporting on the protective effect of antioxidant agents, such as caffeic acid phenethyl ester [5], D-methionine [6], dexamethasone [7], neurotropines [8], flunarizine [9], amifostine [10], N-acetyl cysteine [11,12], erdosteine [13], salicylates [14], gingko biloba extract [15], allopurinol, ebselen [16], resveratrol [4,17], thymoquinone [18], betaglucan [19], and lycopene [20].…”