Malondialdehyde level measurement

Plasma malondialdehyde-like material, an indicator of lipid peroxidation, is increased in conditions of ischaemia, such as stroke [83, 84] and myocardial infarction [85]. Mitochondria extracted from hearts of vitamin-E-deficient rabbits showed a decreased mitochondrial function and an increased formation of oxygen radicals associated with a reduced superoxide dismutase activity. This was partially reversed by addition of vitamin E in vitro [86]. Measurement of in vitro susceptibility to lipid peroxidation in cardiac muscle from vitamin-E-deficient mice showed a highly significant negative correlation between the concentration of vitamin E and in vitro lipid peroxidation. The results indicate that short-term vitamin E deficiency may expose cardiac muscle to peroxidation injuries [ 87 ]. In rats, treatment for 2 days with isoprenaline increased lipid peroxide activity, as measured by malondialdehyde levels, in the myocardium. Vitamin-E-deficient animals were even more sensitive to this effect, and pretreatment with a-tocopheryl acetate for 2 weeks prevented the effect induced by isoprenaline. The authors [88] propose that free-radical-mediated increases in lipid peroxide activity may have a role in catecholamine-induced heart disease. 

Balb c mice and Wistar rats were used in the experiments. The administration of single doses of 1, 2 and 2 caused mainly necrotic changes in the liver, measured by GPT and histopathology. The extent of necrosis depended on doses and on time of observation (1-4 days after injections). In shorter time interval (2-4 hrs) 1, 2 and 2 caused depletion of hepatic GSH (even up to 10 % of control). 4 and 5 did not generate necrotic changes. Increased GPT activity was observed after 3 doses of fi. Single doses of 4, 5 and fi mostly increased the level of malondialdehyde (MDA-indicator of lipid peroxidation) in the liver. Repeated injections (3-7) of the investigated compounds enhanced the activity of ALA-D or ALA-S in the liver and caused steatosis. 

The aim of the present study was to evaluate the effect of LLLT on oxidative markers in serum and tissue biopsies of healing ulcers before and after the 8th session of an LLLT course of chronic leg ulcer treatment. Oxidative damage was assessed in terms of lipid peroxidation reflected by serum malondialdehyde (MDA) level, protein oxidation was measured in terms of tissue protein carbonyls (PCb), and DNA damage was measured in terms of DNA fragmentation. Antioxidative activity was estimated by measuring activity of SOD, GPX and CAT enzymes. 

In the UVB study we also measured malondialdehyde, a marker of lipid peroxidation, but were unable to detect any increase in response to UV light, in contrast to other reports. There are a number of possible explanations. In our experiment, a-tocopherol levels remained high after irradiation, and it is known that lipid peroxidation does not begin in in vitro membrane systems until a-tocopherol is completely depleted [29], Several studies have shown a time lag of one to several hours after irradiation to occur before a measurable increase in cutaneous lipid peroxidation can be detected [26-28] since skin was processed immediately in our experiments, lipid peroxidation may not have reached detectable limits. Finally, the TBARS assay for malondialdehyde is notoriously fraught with artifact and has a relatively high background [30], and noise levels may simply have been too high to detect peroxidation. Results... 

An eight week randomized placebo-controlled intervention study reported on the antioxidant status of lead factoiy workers drinking traditional/fermented rooibos (76). The modulation of oxidative status of these workers was shown by a decreased level of lipid peroxidation (measured as malondialdehyde in the plasma) and increased level of blood glutathione (GSH). The authors suggested that rooibos could play a beneficial preventive role in occupationally exposed... 

The flux of hydroxyl radicals, as measured directly by conversion of salicylate to 2,3- and 2,5-dihydroxybenzoic add (formula [177]), was significantly lower in gallium-desferrioxamine-treated retinas of cat eyes subjected to 90 min retinal ischaemia followed by 5 min of reperfusion (Banin et al. 2000). Gallium-desferrioxamine caused a significant reduction, by 2.56-fold, in lipid peroxidation, as reflected by levels of malondialdehyde. Acorbic acid, a natural antioxidant present in the retina, was severely depleted in untreated eyes. In contrast, in gallium-desferrioxamine-treated eyes, levels were 10 times higher than the control. 

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