Antioxidants luminol oxidation

Thus, a comparative analysis of the total antioxidant activity of blood serum water-soluble components for patients with liver disease (ACW), performed on two free radical oxidation models, showed a relatively low correlation of results (r = 0.798). This is due mainly to the difference in the mechanisms of free radical initiation and the possible impact of some blood serum components (especially proteins) on the process and the rate of initiation. Stronger this effect is manifested in the model Hb-H O, where an active OH -radical-initiator reacts with a number of serum components. The discrepancy in measurement results significant for patients with abnormally high content of certain blood serum components which are differentially inhibit the luminol oxidation due to side reactions. In this regard, more preferred for clinical use to estimate the AOA should be considered the oxidation model with ABAP initiator. Therefore, for further study the correlations of antioxidant and some general clinical parameters of blood serum for patients with liver pathology was chosen the device minilum with this model. 

Figure 4. Antioxidant capacity and lipid oxidation in plasma of volunteers consuming different amounts of procyanidin-rich dark chocolate (6.9 mg of procyanidins per g of chocolate). Antioxidant capacity was evaluated by the ability of plasma to inhibit luminol-dependent chemiluminescence and lipid oxidation by plasma TEARS. Plasma epicatechin concentrations are the average amount of epicatechin determined two hours after chocolate consumption. Ordinate values indicate increases over basal levels of plasma antioxidant capacity (white bars), or decrease over basal values for TEARS (gray bars).

Ascorbic acid is the major water-soluble antioxidant present in cells and plasma. It will quench reactive oxygen species as 02 (Nishikimi 1975), HO (Bielski et aL 1975), and O2 (Bodannes and Chan 1979). On the other hand, it reduces Fe to Fe and thus will stimulate Fenton catalysis of H2O2 —> HO. Hydroperoxide-dependent lipid peroxidation in rat liver microsomes was enhanced by ascorbic acid (Laudicina and Marnett 1990). Ascorbic acid protected cardiac microsomes against lipid peroxidation and oxidative damage (Mukhopadhyay et al. 1993). It diminished both luminol- and lucigenin-amplified H2O2 derived chemiluminescence in concentrations > 10" (Klinger et al. 1996). 

The comparative analysis of the total antioxidant activity of blood serum water-soluble components for patients with liver disease (ACW), performed on two free radical oxidation models Hb-H202 luminol and ABAP- luminol showed, that more preferred for clinical use should be considered the oxidation model with ABAP initiator. 

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