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. All these aspects are focused on the necessity to defend mtDNA against damage. Protecting mechanisms involve the regulation of mitochondrial transport of nucleic acids, and the development of antioxygen defense as preventive measures. In the first case an exclusive role is supposed to play the mitochondrial benzodiazepine receptor and components, regulating the activity of its participants (mitochondrial porin and adenine nucleotide translocator). The possible transport of nucleic acids through Ca(2+)-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-mitochondrial exchange. The second aspect reviews the possible complex of measures to lower the harmful effect of oxygen. Among these measures are mild uncoupling, the opening of a permeability transition pore and cellular apoptosis as was recently suggested by Skulachev. Problems such as cellular aging and mitochondrial diseases, are discussed in light of the relevance to the problem of oxidative stress.