ABSTRACT
In connection with the term ‘‘oxidative stress,’’ we consider ‘‘loose coupling/ uncoupling’’ in relation to mitochondria.
In pathophysiology, ‘‘oxidative stress’’ basically means an imbalance of redox potential accompanied by a surplus of partially reduced oxygen atoms, for example, O2•, which to a great extent has used up the reduced forms of cellular defense, i.e., glutathione 2 RSH → RSSR. In other cases, the oxidation of reduced glutathione is not in the foreground. Further antioxidative enzymatic systems, i.e., glutatione peroxidase, superoxide dismutase, and catalase, and, apart from vitamins C and E and provitamin carotene, other thiol-containing smaller molecules, thioredoxin, and lipoic acid take part in the multifold scenery. Thioredoxin peroxidase has recently been added to this arsenal (1). But even this pool may become exhausted.
