Ramkumar Vickram, Whitworth Craig A, Pingle Sandeep C, Hughes Larry F, Rybak Leonard P
Department of Pharmacology, Southern Illinois University School of Medicine, P.O. Box 19620, Springfield, IL 62794-9620, USA.
Hear Res. 2004 Feb;188(1-2):47-56. doi: 10.1016/S0378-5955(03)00344-7.
Adenosine plays a major cytoprotective role during ischemia and conditions of oxidative stress. Previous studies in our laboratory indicate that oxidative stress induces expression of the A1 adenosine receptor (A1AR) via activation of nuclear factor (NF)-kappaB. In this study, we tested whether noise exposure could induce oxidative stress and determine whether this induces expression of the A1AR in the chinchilla cochlea. Chinchillas were exposed to a 96 dB 4 kHz octave band of noise for 6 h of daily exposure, followed by an 18 h noise-free period. This noise paradigm resulted in threshold shifts of 10-60 dB over the frequency range (1-16 kHz) tested. Radioligand binding studies for the A1AR indicate a significant increase in receptor ( approximately 2-fold) expression soon after the first noise exposure period (usually within approximately 8 h of the initiation of noise), which gradually returned to basal levels by day 7. The rise in A1AR levels was followed by a significant increase in malondialdehyde levels by day 3, which also recovered by day 7. Assessment of the activity of NADPH oxidase in the cochlea indicates a significant increase in enzyme activity which was evident by approximately 8 h following initiation of noise exposure, and which persisted for at least up to day 3. Electrophoretic mobility shift assays indicate that the increase in A1AR was associated with a significant increase in NF-kappaB activity following noise exposure. We conclude that noise exposure induces A1AR expression, which might be mediated, in part, through generation of reactive oxygen species and activation of NF-kappaB.
腺苷在缺血和氧化应激条件下发挥着主要的细胞保护作用。我们实验室之前的研究表明,氧化应激通过激活核因子(NF)-κB诱导A1腺苷受体(A1AR)的表达。在本研究中,我们测试了噪声暴露是否会诱导氧化应激,并确定这是否会诱导灰鼠耳蜗中A1AR的表达。将灰鼠每天暴露于96 dB 4 kHz倍频程噪声中6小时,随后有18小时的无噪声期。这种噪声模式导致在测试的频率范围(1-16 kHz)内阈值偏移10-60 dB。对A1AR的放射性配体结合研究表明,在首次噪声暴露期后不久(通常在噪声开始后约8小时内),受体表达显著增加(约2倍),到第7天逐渐恢复到基础水平。A1AR水平升高后,丙二醛水平在第3天显著增加,到第7天也恢复正常。对耳蜗中NADPH氧化酶活性的评估表明,酶活性显著增加,在噪声暴露开始后约8小时明显,至少持续到第3天。电泳迁移率变动分析表明,噪声暴露后A1AR的增加与NF-κB活性的显著增加有关。我们得出结论,噪声暴露诱导A1AR表达,这可能部分是通过活性氧的产生和NF-κB的激活介导的。