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 forĀ oxidative stress?
High quality evidence finds medium-sized reductions in glutathione and glutathione peroxidase levels in people with schizophrenia compared to controls, and no differences in glutathione disulfide or gluthatione reductase levels.
In people with first-episode psychosis, moderate quality evidence finds large reductions in total antioxidant levels in plasma or serum compared to controls.
In people with acute relapse of psychosis there are decreases in catalase, superoxide dismutase, and glutathione peroxidase in red blood cells.
In stable outpatients with schizophrenia, moderate quality evidence finds medium-sized reductions in superoxide dismutase in red blood cells, and medium to large increases in superoxide dismutase in serum. There are also increases in thiobarbituric acid reactive substances in serum, catalase in red blood cells, and nitrate in plasma of stable outpatients. There are no differences in thiobarbituric acid reactive substances in plasma or glutathione peroxidase in red blood cells.
In chronic inpatients, moderate quality evidence suggests a large effect of increased malondialdehyde in plasma. There are 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 are 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 (<18 years), moderate quality evidence finds no differences in catalase, glutathione, glutathione peroxidase, superoxide dismutase, total antioxidant status or cell/DNA oxidative damage when compared to age-matched controls.
October 2020
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Podcast Library
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