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SIIA Público
SISTEMA INTEGRAL DE INFORMACIÓN ACADÉMICA - PÚBLICO
Título del libro: Free Radicals And Diseases Título del capítulo: Oxygen: From Toxic Waste to Optimal (Toxic) Fuel of Life
Some 2.5 billion years ago, the great oxygenation event (GOE) led to a
105-fold rise in atmospheric oxygen [O-2], killing most species on
Earth. In spite of the tendency to produce toxic reactive oxygen species
(ROS), the highly exergonic reduction of O-2 made it the ideal
biological electron acceptor. During aerobic metabolism, O-2 is reduced
to water liberating energy, which is coupled to adenosine triphosphate
(ATP) synthesis. Today, all organisms either aerobic or not need to deal
with O-2 toxicity. O-2-permeant organisms need to seek adequate [O-2],
for example, aquatic crustaceans bury themselves in the sea bottom where
O-2 is scarce. Also, the intestinal lumen and cytoplasm of eukaryotes is
a microaerobic environment where many facultative bacteria or
intracellular symbionts hide from oxygen. Organisms such as plants,
fish, reptiles and mammals developed O-2-impermeable epithelia, plus
specialized external respiratory systems in combination with O-2-binding
proteins such as hemoglobin or leg-hemoglobin control [O-2] in
tissues. Inside the cell, ROS production is prevented by rapid O-2
consumption during the oxidative phosphorylation (OxPhos) of ATP. When
ATP is in excess, OxPhos becomes uncoupled in an effort to continue
eliminating O-2. Branched respiratory chains, unspecific pores and
uncoupling proteins (UCPs) uncouple OxPhos. One last line of resistance
against ROS is deactivation by enzymes such as super oxide dismutase and
catalase. Aerobic organisms profit from the high energy released by the
reduction of O-2, while at the same time they need to avoid the toxicity
of ROS.