Preventive effect of magnesium supplement on noise-induced hearing loss in the guinea pig

被引:24
作者
Scheibe, F
Haupt, H
Ising, H
机构
[1] Humboldt Univ, Charite Hosp, Dept Otorhinolaryngol, D-10117 Berlin, Germany
[2] Fed Environm Agcy, Inst Water Soil & Air Hyg, D-14195 Berlin, Germany
关键词
magnesium supplement; impulse noise; hearing loss; auditory brain stem response testing; guinea pig;
D O I
10.1007/PL00007505
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
The effect of magnesium (Mg) on noise-induced hearing loss was investigated in two groups of adult pigmented guinea pigs maintained either on optimal or suboptimal (physiologically high or low) Mg produced by different diets. The total Mg concentrations of the perilymph (PL), cerebrospinal fluid, blood plasma and red blood cells were measured by atomic absorption spectrometry and were found to differ significantly between the two groups (P < 0.01). One ear of each animal was exposed to either a single shooting impulse at a peak pressure level of 187 dB or two impulse noise series at a rate of 1/s and peak pressure levels of 150 dB (1,000 impulses) and 167 dB (2,280 impulses), respectively. Temporary (TTS) and permanent (PTS) hearing threshold shifts in anesthetized animals were measured 2 h and 1 week after the noise exposure, using auditory brain stem response (ABR) audiometry at a frequency range from 3.75 to 30 kHz. Exposure to the single noise impulse resulted in a mean TTS that was significantly lower in the high ME group than that in the low Mg group (P < 0.05), although no substantial PTS was observed in either group. In the animals exposed to 150 dB noise, the TTS showed a tendency towards an Mg-related reduction at the higher frequencies. A small difference in PTS was found between the low Mg and high Mg groups, but was not significant. Exposure to the 167-dB noise series caused a considerable TTS, which was significantly lower in the high Mg group at 7.5 and 15 kHz than in the low Mg group (P < 0.05). The mean PTS showed a significant difference between the two Mg groups over the whole frequency range (P < 0.05) and was found to correlate negatively with the total Mg concentrations of both PL and plasma (P < 0.05). Moreover, the high Mg group showed a faster recovery from the hearing threshold shift than the low Mg group. The present findings show that preventive oral Mg supplements can significantly reduce the rate of acoustic trauma caused by high-level impulse noise exposure in the guinea pig.
引用
收藏
页码:10 / 16
页数:7
相关论文
共 33 条
[1]   MAGNESIUM-DEFICIENCY AND HYPERTENSION - CORRELATION BETWEEN MAGNESIUM-DEFICIENT DIETS AND MICROCIRCULATORY CHANGES INSITU [J].
ALTURA, BM ;
ALTURA, BT ;
GEBREWOLD, A ;
ISING, H ;
GUNTHER, T .
SCIENCE, 1984, 223 (4642) :1315-1317
[2]   NOISE-INDUCED HYPERTENSION AND MAGNESIUM IN RATS - RELATIONSHIP TO MICROCIRCULATION AND CALCIUM [J].
ALTURA, BM ;
ALTURA, BT ;
GEBREWOLD, A ;
ISING, H ;
GUNTHER, T .
JOURNAL OF APPLIED PHYSIOLOGY, 1992, 72 (01) :194-202
[3]   ORAL MAGNESIUM INTAKE REDUCES PERMANENT HEARING-LOSS INDUCED BY NOISE EXPOSURE [J].
ATTIAS, J ;
WEISZ, G ;
ALMOG, S ;
SHAHAR, A ;
WIENER, M ;
JOACHIMS, Z ;
NETZER, A ;
ISING, H ;
REBENTISCH, E ;
GUENTHER, T .
AMERICAN JOURNAL OF OTOLARYNGOLOGY, 1994, 15 (01) :26-32
[4]  
ATTIAS J, 1998, ADV NOISE RES, V1, P271
[5]   Diltiazem does not protect the ear from noise-induced hearing loss in Mongolian gerbils [J].
Boettcher, FA .
LARYNGOSCOPE, 1996, 106 (06) :772-776
[6]   Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function [J].
Clerici, WJ ;
Yang, LH .
HEARING RESEARCH, 1996, 101 (1-2) :14-22
[7]  
Devriere F., 1991, Journal d'Acoustique, V4, P363
[8]   RECEPTOR PHARMACOLOGICAL MODELS FOR INNER-EAR THERAPIES WITH EMPHASIS ON GLUTAMATE RECEPTORS - A SURVEY [J].
EHRENBERGER, K ;
FELIX, D .
ACTA OTO-LARYNGOLOGICA, 1995, 115 (02) :236-240
[9]  
ERNST E, 1990, Z ALLGEMEINMED, V66, P637
[10]   Magnesium reduces free radicals in an in vivo coronary occlusion-reperfusion model [J].
Garcia, LA ;
Dejong, SC ;
Martin, SM ;
Smith, RS ;
Buettner, GR ;
Kerber, RE .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 32 (02) :536-539