Desai Varsha G, Fuscoe James C
Center for Functional Genomics, Division of Systems Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, 3900 NCTR Road, HFT-130, Jefferson, AR 72079, USA.
Mutat Res. 2007 Mar 1;616(1-2):210-2. doi: 10.1016/j.mrfmmm.2006.11.011. Epub 2006 Dec 18.
It is well documented that mitochondrial dysfunction significantly contributes to a number of degenerative diseases, metabolic disorders, and drug- and chemical-induced toxicities. Thus far, information gained by several molecular and biochemical techniques used to delineate the mechanism of impaired mitochondrial activity underlying different diseases and various toxicities is still limited due to their low throughput potential. Here, we describe the development of mitochondria-specific mouse oligonucleotide microarray and its potential to define mechanisms of disease progression and drug toxicities associated with mitochondrial dysfunction at both nuclear and mitochondrial genome level.
线粒体功能障碍显著导致多种退行性疾病、代谢紊乱以及药物和化学物质诱导的毒性,这一点已有充分的文献记载。迄今为止,用于阐明不同疾病和各种毒性背后线粒体活性受损机制的多种分子和生化技术所获得的信息,由于其低通量潜力,仍然有限。在此,我们描述了线粒体特异性小鼠寡核苷酸微阵列的开发及其在核基因组和线粒体基因组水平定义与线粒体功能障碍相关的疾病进展和药物毒性机制的潜力。