| 摘要 |
This invention relates to methods for detecting and quantitating a heteroplasmic mutation at position 12027 of mitochondrial DNA in various human tissues. The mutation is a <I>t</I> T <I>c</I> substitution that changes the protein structure of NADH-Ubiquinone reductase causing oxidative stress by increased superoxide production and reduced electron transfer. The mutant form predominates in 24% of the mtDNA in lymphocytes from normals and in 47% of a sample of 180 schizophrenics. Several other illnesses such as cancer, cardiovascular disorder and age related neurological, ophthalmological and dermatological age related degeneration are also associated with oxidative stress. The invention thus affords methods of predicting the likelihood of schizophrenia and other ailments before the onset of clinical symptoms. Also disclosed are methods of alleviating the illnesses caused by the mutation by replacing mtDNA or preventing its expression and methods of using quercetin and its glycosides to reduce superoxide emission without compromising the energy transfer capabilities of the reductase. |
