Abstract
Living with oxygen is basically unsafe, but vital. During evolution, oxygen originally a waste product of the metabolism in primitive unicellular organisms became normal product of the metabolism in higher animal species involving humans.
Even when oxidative reactions are toxic, and destructive, they are tolerated by all organisms to some extent. The fact has opened the discussion about efficiency of antioxidant mechanisms.
The classical enzyme antioxidant defence alone does not explain high tolerance of the organism for oxygen. Moreover, enzyme antioxidant mechanisms are not hundred percent effective in preventing oxidation what allows oxidative damage to continue.
The pathogenesis of autoimmune joint inflammatory diseases is related to activation of native immune system. At site of inflammation, activated neutrophils and macrophages consume large amounts of oxygen, whose corollary is the increase of reactive oxygen species (ROS) production.
There are several mechanisms how oxidative stress is involved into the pathogenesis of autoimmune joint inflammatory diseases. Excess production of ROS in the joint area encourages process of re-oxygenation, which then promotes joint inflammation.
ROS further inhibit connective tissue cell proliferation, in some cases ROS have been shown to induce cell death to these cells inducing apoptosis