Urinary 8-epi-prostaglandin (PG) F20 |
Levels 0.5-3.0 ng/ml are normal Note: 1 ml urine, ELISA |
The prostaglandin derivate 8-epi-prostaglandin PG-F20 has most significance as sensitive and specific marker of lipid peroxidation. The formation of this isoprostane out of arachidonic acid is catalyzed through free radicals and has strong vasoconstrictive and mitogenic effects. Higher concentrations of 8-iso-PGF20 are associated with a disturbed radicals homeostasis and oxidative disruption of the prostaglandin synthesis. The renal excretion rate correlates with the number of smoked cigarettes, chemical exposure, plasma lipids (cholesterol), the activity of chronically inflammatory processes, like arteriosclerosis, Alzheimer, and diabetes, as well as with the oxidative burden in kidney insufficiency. The success of oral anti-oxidative interventions is reliable measurable after a couple of weeks supplementing antioxidants, such as vitamin C |
Serum malondialdehyde (MDA) |
Levels 0.36-1.4 µmol/mmol are normal |
MDA is a reactive degradation product with the peroxidation of lipids. It is significantly involved with the oxidation of LDL cholesterol.
MDA is mostly renally excreted and clearly less sensitive compared to 8-iso-PGF20
1 ml ETDA, urine, HPLC |
Urinary malondialdehyde |
Levels 0.2-1.45 µmol/mmol creatinine are normal |
Urinary 4-hydroxynonenal (4-HNE) |
Levels < 50 nmol/l are normal |
4-HNE is formated during the peroxidation of polyunsaturated fatty acids (e.g. linoleic and arachidonic acid). Because of its two functional groups (aldehyde and hydroxyl) as well as the C=C double bound it is considered one the most reactive auto-oxidative products. 4-HNE is mostly renally excreted 3 ml EDTA, HPLC |
Serum oxidative modified LDL cholesterol (oxLDL) |
Levels < 6.0 U/ml are normal, or oxLDL antibody: negative |
Oxidative modified LDL (ox-LDL) has a highly arterogenic potential. The measurement is direct or via the determination of antibodies against oxLDL serum, ELISA |
Total anti-oxidative capacity (TAC) |
Levels 1.3-1.7 mmol/l are normal0.5 ml native serum |
General screening parameter for evaluation of antioxidants status. TAC gives the ability of the sample material to quench free radicals The oxidation of ABTS with H2O2 and the ABTS+ The added sample inhibits the coloring reaction according to its antioxidant content. Photometric determination at 600 nm |
Urinary 8-hydroxy-2'-deoxyguanosine (8-oxo-dG) |
Levels 0.5-1.7 / 0.4-1.4 nmol/mmol creatinine (female / male) are normal |
The oxidative DNA damage causes formation of fragments like 8-hyroxy-2'-deoxyguanosine (8-oxo-dG) in urine which can be demonstrated by auto-antibodies against oxidated DNA bases Note: morning urine, fluorescence or ELISA |
Whole blood superoxide dismutase total activity (SOD) |
Levels 130-505 U/ml are normal |
SOD reduces the super-oxide anion radical into hydrogen.peroxide and lipid-hydro-peroxide. In hypochondria manganese dependent, in cytosol (liquid found inside cells) copper/zinc dependent |
Whole blood glutathion peroxidase total activity (GSH-Px) |
Levels 4170-10880 U/ml are normal |
Selenium dependent GSH-Px reduces the hydroperoxide and lipidhydroperoxide |
Serum glutathione (GSH) |
Levels 2.4-4.4 µmol/l are normal |
A decrease in cellular glutathione concentrations has negative effects on various cells of the immune system. Particularly cytotoxic T-cell activity, T-cell proliferation, the generation of CD-8 + T-cell blasts as well as the lymphkin activating killer cells and NK-cells are affected from l-glutathione depletion.
Note: Additionally the activity of GSH-S-transferases and GSH:GSSG quotient as well as selenium status assist the diagnosis The cellular glutathione content can be measured by flow cytometry |
Serum glutathione disulfide (GSSG) |
Levels < 0.5 µmol/l are normal |
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Serum glutathione / glutathion disulfide (GSH/GSSG) quotient |
Ratios 10-15 U/ml are normal |
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Erythrozytes glutathione (GSH) |
Levels 785-1075 µmol/l are normal |
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Lymphocytes glutathione (GSH) |
Levels 350-650 MI are normal |
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Whole blood glutathione (GSH) |
Levels 4170-10880 U/ml are normal |
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Plasma glutamine |
Levels 600-900 µmol/l are normal, < 600 µmol/l indicate deficiency |
Glutamine is with a percentage of 20% quantitative the most significant amino acid in blood plasma. In skeletal muscle over 60% of the free amino acids pool consists of glutamine. Causes of glutamine depletion for critically ill are: increased muscle/protein wasting, increased requirement of mucosa, liver and immunocompetent cells |
Asymmetric dimetylarginine (ADMA) |
Levels 0.3-0.7 µmol/l are normal |
Asymmetric dimetylarginine is a endogenous, competitive inhibitor of endothelial NO -synthase (eNOS) and is usually degraded by dimethylarginine-dimethylaminohyrolase. Oxidative stress and Hcy inhibit this enzyme, whereby ADMA levels rise. Raised ADMA levels are found with hypercholesterolaemia, hyperhomocysteinemia, diabetes, PAVD, preeclampsia, erectile dysfunction and kidney dysfunction. ADMA is today seen as a independent risk factor for cardiovascular disease. The balance between ADMA and l-arginine can be restored by raising l-arginine levels |
Plasma arginine |
Levels < 100 µmol/l are normal |
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ADMA / arginine quotient |
Ratios 50-100 are normal |
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CoQ10 red / CoQ10 ox quotient |
Ratio of about 90-10 is optimal |
The relation of reduced Coenzym Q10 (ubiquinol CoQ10 red) to oxidized Coenzym Q10 (ubiqinone, CoQ10 ox) is a meaningful and sensitive parameter for lipid peroxidation and oxidative stress |
Further parameters |
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Homocysteine (plasma), hs-CRP, selenium (whole blood), vitamin E |