Oxidative stress
What is oxidative stress?
While oxygen is a vital component of life, some oxygen-based compounds called free radicals can be toxic due to their highly unstable nature. The key free radical classes are the reactive oxygen species (ROS) and reactive nitrogen species (RNS), and they are formed as by-products of normal metabolism. Under normal conditions, these free radicals are tightly monitored and controlled by stringent protective barriers, such as their rapid removal from cells; and antioxidant enzymes that break them down. At these tightly maintained concentrations, free radicals play an important role in cellular signalling, immune responses and cell growth. However, excess free radicals can result from interruption of the antioxidant defense barrier, or from excess production. This can cause oxidative stress, resulting in structural damage to cellular proteins, fats, carbohydrates and nucleic acids (DNA and RNA). Severe oxidative stress can result in failure of cell growth, apoptosis and cell necrosis.
What is the evidence for oxidative stress?
In people with first-episode psychosis, moderate quality evidence found medium-sized decreases in catalase and superoxide dismutase in red blood cells, and decreases in nitrate and uric acid in plasma. There were medium to large increases in superoxide dismutase, malondialdehyde, and thiobarbituric acid reactive substances in plasma. There were no differences in glutathione peroxidase levels. In people with acute relapse of psychosis there were decreases in catalase, superoxide dismutase, and glutathione peroxidase in red blood cells.
In stable outpatients with schizophrenia, moderate quality evidence found medium-sized effects of reduced superoxide dismutase in red blood cells, and medium to large effects of increased superoxide dismutase in serum. There were also increases in thiobarbituric acid reactive substances in serum, catalase in red blood cells, and nitrate in plasma of stable outpatients. There were no differences in thiobarbituric acid reactive substances in plasma or glutathione peroxidase in red blood cells. High quality evidence found a small decrease in glutathione in the anterior cinguate of people with schizophrenia.
In chronic inpatients, moderate quality evidence found a large effect of increased malondialdehyde in plasma. There were medium to large effects of decreased catalase in both red blood cells and plasma, decreased vitamins C and E in plasma, decreased glutathione peroxidase in both red blood cells and plasma, and decreased superoxide dismutase in plasma. There were no differences in superoxide dismutase in red blood cells, or thiobarbituric acid reactive substances or uric acid in plasma.
In people with early-onset schizophrenia (onset <18 years), moderate quality evidence found no differences in catalase, glutathione, glutathione peroxidase, superoxide dismutase, total antioxidant status or cell/DNA oxidative damage compared to age-matched controls.
December 2019
Fact Sheet Technical Commentary
Green - Topic summary is available.
Orange - Topic summary is being compiled.
Red - Topic summary has no current systematic review available.