ABSTRACT
Together with xanthine oxidase (XO), NADPH oxidases (Noxs), and nitric oxide synthases (NOSs), mitochondria is one of the major producers of reactive oxygen (ROS) and nitrogen (RNS) species. These enzymes and mitochondria are not only major producers of free radicals in cells and tissues but generate them as signaling species in many enzymatic reactions, and not only as the initiators of numerous damaging processes. The major distinction of mitochondria from the enzymes just mentioned is uncertainty of mode and means of production of oxygen and nitrogen radicals. At present, there are seemingly no doubts that mitochondrial superoxide (O2·−) production is not an in vitro artifact but a phenomenon observed in in vivo systems. (However, it should be noted that there are some objections concerning the actual levels of O2·− production by mitochondria in vivo [1]). O2·− is a major ROS produced in mitochondria as a result of a leak of electrons from the two-electron transport respiratory mitochondrial chain to the one-electron reduction of dioxygen, and may be the source of damage in normal biological processes. This is a very important function of O2·−, but up-to-date studies also highlight the important signaling activity of mitochondria-producing O2·− in many enzymatic processes. We will now consider the mechanisms of O2·− production by mitochondria.
