The unceasing need for oxygen is in contradiction to the fact that it is in
fact toxic to mammals. Namely, its monovalent reduction can have as a
consequence the production of short-living, chemically very active free
radicals and certain non-radical agents (nitrogen-oxide,
superoxide-anion-radicals, hydroxyl radicals, peroxyl radicals, singlet
oxygen, peroxynitrite, hydrogen peroxide, hypochlorous acid, and others).
There is no doubt that they have numerous positive roles, but when their
production is stepped up to such an extent that the organism cannot eliminate
them with its antioxidants (superoxide-dismutase, glutathione-peroxidase,
catalase, transferrin, ceruloplasmin, reduced glutathion, and others), a
series of disorders is developed that are jointly called ?oxidative stress.?
The reactive oxygen species which characterize oxidative stress are capable
of attacking all main classes of biological macromolecules, actually
proteins, DNA and RNA molecules, and in particular lipids. The free radicals
influence lipid peroxidation in cellular membranes, oxidative damage to DNA
and RNA molecules, the development of genetic mutations, fragmentation, and
the altered function of various protein molecules. All of this results in the
following consequences: disrupted permeability of cellular membranes,
disrupted cellular signalization and ion homeostasis, reduced or loss of
function of damaged proteins, and similar. That is why the free radicals that
are released during oxidative stress are considered pathogenic agents of
numerous diseases and ageing. The type of damage that will occur, and when it
will take place, depends on the nature of the free radicals, their site of
action and their source.
Purification of protein–DNA complexes by native gel electrophoresis for electron microscopy study
