Ototoxic interaction between noise and pheomelanin: distortion product otoacoustic emissions after acoustical trauma in chloroquine-treated red, black, and albino guinea pigs.
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引用次数: 0
Abstract
This study provides further evidence of an ototoxic interaction between red pheomelanin pigmentation and noise-induced hearing loss. Red, black, and albino guinea pigs were treated with a low, a high, or no dose of chloroquine. The 2f1-f2 distortion product otoacoustic emission (DPOE) measurements were measured before, immediately after, and 1 month after noise exposure to a 1-kHz tone at 105 dB SPL for 72 hours. In red guinea pigs, the DPOE was severely affected by noise trauma when treated even by a low single dose of chloroquine, whereas in both albino and black guinea pigs, the chloroquine effect on the DPOE was temporary and present only when the drug was given in a high single dose. The structure most likely to be responsible for the severe loss of DPOE in chloroquine-treated red animals is the strial melanocyte. The damage may be triggered by an ototoxic noise-induced production of radical oxygen species from pheomelanin, for example, by the Fenton reaction or due to the increased variability of the melanocyte 1 receptor gene as in red-haired individuals.
这项研究提供了进一步的证据,证明红色现象黑色素沉着与噪音性听力损失之间存在耳毒性相互作用。红豚鼠、黑豚鼠和白化豚鼠分别接受低剂量、高剂量或无剂量的氯喹治疗。在105 dB SPL的1 khz噪声下暴露72小时之前、之后和1个月后测量了2f1-f2失真乘积耳声发射(DPOE)。在红色豚鼠中,即使单次低剂量氯喹也会严重影响DPOE,而在白化豚鼠和黑色豚鼠中,氯喹对DPOE的影响是暂时的,只有在单次高剂量给药时才会出现。在氯喹处理过的红色动物中,最可能导致DPOE严重丧失的结构是黑素细胞。损伤可能是由耳毒性噪声引起的由黑色素产生的自由基氧引起的,例如,通过芬顿反应,或者由于黑素细胞1受体基因的变异性增加,如在红发个体中。