MITOCHONDRIAL DAMAGE AS A SOURCE OF DISEASES AND AGING - A STRATEGY OF HOW TO FIGHT THESE

Some aspects of a defense against an oxidative stress are reviewed. Al l these aspects are focused on the necessity to defend mtDNA against d amage. Protecting mechanisms involve the regulation of mitochondrial t ransport of nucleic acids, and the development of antioxygen defense a s preventive measures. In the first case an exclusive role is supposed to play the mitochondrial benzodiazepine receptor and components, reg ulating the activity of its participants (mitochondrial porin and aden ine nucleotide translocator). The possible transport of nucleic acids through Ca2+-dependent permeability transition pore, representing one of the functional states of mitochondrial benzodiazepine receptor, is put forth. Such mechanisms can also cover the genomic nuclear-mitochon drial exchange. The second aspect reviews the possible complex of meas ures to lower the harmful effect of oxygen. Among these measures are m ild uncoupling, the opening of a permeability transition pore and cell ular apoptosis as was recently suggested by Skulachev. Problems such a s cellular aging and mitochondrial diseases, are discussed in light of the relevance to the problem of oxidative stress.