Does overproduction of chaperone proteins favour the repair of DNA injuries induced by oxidative stress? (Mini review)

Genotype resistance to oxidative stress, induced by various physical/chemical stimuli has been the focus of scientists for the last decades, with several aspects – ecological (the formation of the genetic elite of population), agricultural and medical (radio-chemotherapy).

Genotype resistance to oxidative stress is regarded as the integration of different morphological, physiological, biochemical, metabolic and genetic characteristics. Currently, it is supposed that the mechanisms involved in the formation of genotype resistance to oxidative stress are inter-correlated and inter-dependent, comprising changes in genes, proteins, enzymes, different metabolic pathways and/or biological networks. According to the present state of knowledge, various cellular targets, resulting in genotoxic stress, induction of DNA damage, mutations, genomic instability or apoptosis can trigger different signal transduction pathways, activating DNA repair, antioxidant and chaperone defence systems.

Till now, a lot of experimental data have been accumulated concerning the contribution of DNA repair to the formation of genotype resistance to oxidative stress. At the same time, genotype resistance of organisms is largely determined by the ability of molecular chaperones to maintain conformational homeostasis of proteins (folding – misfolding – refolding or aggregation – degradation). The role of chaperones in protein homeostasis and cell death, especially in apoptosis, is well discussed in literature, but much less is known about their function in DNA repair. In this regard, here we addressed the question of whether the overproduction of chaperone proteins contributes to the repair of DNA damage caused by oxidative stress.