Oxidative stress is implicated in a large number of diseases, including neurodegenerative diseases and autoimmune diseases.
Indicators of oxidative stress have been detected in muscles and blood of CFS patients. Oxidative damage to cellular membranes can alter the permeability of the blood-brain barrier, which could lead to some of the cognitive symptoms observed in patients. Increased oxidative stress in CFS could have several origins: chronic inflammation (activated neutrophils release pro-oxidative molecules), excess nitric oxide production (NO reacts with free radicals to produce peroxynitrite, a potent oxidant), or exposure to environmental toxins (exposure to certain chemicals leads to the depletion of essential antioxidants such as glutathione and selenium; heavy metals can also directly inhibit antioxidant enzymes like superoxide dismutase or glutathione reductase).
Oxidative stress markers are useful to evaluate the need for antioxidant therapy.
Useful tests for oxidative stress assessment include the following:
- Total antioxidant capacity in serum
- IgA/IgM against oxidative and nitrosative products
- Fatty acids oxidation (MDA/TBARS)
TOTAL ANTIOXIDANT CAPACITY
Antioxidant systems in the body normally limit the extent of oxidative damage, however a number of factors can severely affect their function (exposure to environmental toxins, disease, nutritional deficiencies). There are many types of antioxidant systems, including enzymes that detoxify reactive oxygen molecules, proteins that chelate metals, small molecules that scavenge radicals. Although measurement of single antioxidants may be needed in some cases, a best index in oxidative stress studies is to measure the total antioxidant capacity of a sample, that shows the overall effect of multiple antioxidants working together.
We perform a colorimetric assay that measures the total antioxidant capacity of a sample (e.g., serum), based on the reduction of Cu++ to Cu+.
IgA/IgM OXIDATIVE PRODUCTS
Chronic diseases, neurodegenerative and auto-immune diseases are associated with the production of antibodies, mainly IgA and IgM, directed against proteins modified by the action of nitrosative stress (reaction of specific amino-acids with nitric oxide or peroxynitrite).
More specifically, the assay will look for antibodies directed against the following antigens:
- NO-cysteine
- NO2-tyrosine
- NO-BSA
- NO-tryptophane
- NO-arginine
- Azelaic acid
- Malondialdehyde
Detection of these antibodies provides information on the pathogenesis of the disease and its evolution. Measurement of antibodies against azelaic acid and malondialdehyde evaluates the level of lipoperoxidation.
MDA-TBARS, FATTY ACIDS OXIDATION
Lipid peroxidation is a well-defined mechanism of cellular damage. Lipid peroxides decompose to form compounds such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), natural end-products of lipid peroxidation. Measuring these end-products is one of the most widely accepted assays for determination of oxidative damage. One approach to quantify MDA in a serum sample uses the capacity of MDA to react with thiobarbituric acid (TBA), forming an MDA-TBA adduct that can be quantified spectrophotometrically.