Malondialdehyde, formation

The diterpenes andrographolide, andrographiside and neoandro-grapholide isolated from A. paniculata were also investigated for their protective effects on hepatotoxicity induced in mice by carbon tetrachloride or /ert-butylhydroperoxide ( BHP) intoxication by Kapil et pretreatment of mice with the individual diterpenes at a dose of 100 mg/kg, i.p. for 3 consecutive days were observed to produce significant reduction in malondialdehyde formation, reduced glutathione (GSH) depletion and... 

The concentration of ozone taken up by the media containing linolenic acid is plotted against time after addition in Figure 8. The rate of ozone breakdown is constant (ozone uptake linear with time) for the first two min until about 0.12 ml ozone are absorbed and then the rate decreases sharply, reaching a steady-state rate of ozone uptake between 10-12 min. This first break in the curve corresponds to an ozone uptake of 0.12 ml + (24 moles/liter) = 0.005 millimoles (or 10 M). This is equivalent to 1 mole of linolenic acid added per mole ozone absorbed. Thiobarbituric acid reactant production is also plotted on the same axis. This compound (TBA reactant) probably arises by formation of a three-carbon fragment (malondialdehyde) from the ozone-induced oxidation of linolenic acid (23). The rate of TBA reactant formation is also linear for the first 2 min at which point the curve undergoes a less pronounced break. Malondialdehyde formation ceases immediately when the ozone is shut off (Scrub 1 on). An oxygen control sample produced no malondialdehyde. 

Yano E. 1988. Mineral fiber-indueed malondialdehyde formation and effects of oxidant scavengers in phagocytic cells. Int Arch Occup Environ Health 61 19-23. 

However, work in hepatocytes suggested that acetaminophen toxicity may involve iron-mediated oxidative stress. Albano and coworkers (Albano et al. 1983) reported that incubation of acetaminophen with cultured mouse hepatocytes or with polycyclic aromatic hydrocarbon-induced rat hepatocytes produced oxidative stress as indicated by peroxidation of lipids (malondialdehyde formation). Moreover, the importance of iron in the toxicity of acetaminophen has been shown in both rat and mouse hepatocytes by numerous investigators (Adamson and Harman 1993 Ito et al. 1994 Kyle et al. 1987). Collectively, these data... 

Intraperitoneal administration of 120 pg ochratoxin A/kg bw per day to Wistar rats, for 10, 30 or 60 days, produced oxidative stress and doseAime-related apoptosis in both proximal and distal epithelial kidney cells. Ochratoxin A concentrations in the kidneys were proportional to the time of exposure and amounted to 547, 753 and 930 ng/g kidney tissue after 10, 30 and 60 days, respectively. Oxidative stress was evident from increased malondialdehyde formation in the kidney cells (Petrik et al., 2003). 

Lipid peroxidation Malondialdehyde formation Lipofuscin pigment concentration Superoxide dismutases mitochondrial cytosolic... 

Ichinose T, Miller M, Shibamoto T (1994) Inhibition of Malondialdehyde Formation from Liver Microsomes by a Lichen Constituent. Food Chem Toxicol 32 1167... 

An interesting variation of this procedure relies upon the formation of malondialdehyde precursors in situ. Vinylogs of Vilsmeier-Haack intermediates (60), formed from dimethylaminoacroleins (59) and phosgene, undergo reaction with 2,4,6-triaminopyrimidine to yield 6-alkyl- and 6-aryl-substitutcd 2,4-diaminopyrido[2,3-d]-pyri-midines (61). Dimethylaminoacroleins were found to be unsatisfactory. ... 

The reactions described so far do not require the involvement of the apo-B protein, neither would they necessarily result in a significant amount of protein modification. However, the peroxyl radical can attack the fatty acid to which it is attached to cause scission of the chain with the concomitant formation of aldehydes such as malondialdehyde and 4-hydroxynonenal (Esterbauer et al., 1991). Indeed, complex mixtures of aldehydes have been detected during the oxidation of LDL and it is clear that they are capable of reacting with lysine residues on the surface of the apo-B molecule to convert the molecule to a ligand for the scavenger receptor (Haberland etal., 1984 Steinbrecher et al., 1989). In addition, the lipid-derived radical may react directly with the protein to cause fragmentation and modification of amino acids. 

Further enhancement in specificity has been achieved by the HPLC separation of the complex prior to measurement (Shih and Hu 1999). Other possible approaches are the extraction of malondialdehyde prior to the formation of the chromogen and/or derivative spectrophotometry. 

Other indices measure a secondary stage of oxidation, such as the anisidine value (ANV), pointing to formation of carbonyl compounds, capable of undergoing condensation reactions with p-anisidine, and the thiobarbituric acid reactive substance (TBARS) pointing to the presence of malondialdehyde (MDA) in particular. In biological systems, TBARS is of widespread use as a measure for the extent of oxidation damage. Another test for stability of oils to oxidation is based on the development of acidity as secondary product, for example, standards using the Rancimat equipment or a similar setup. 

Antioxidant activity was also tested in a liver microsome system. In this study, mice were treated by oral intubation (2 times/wk) with 0.2 ml olive oil alone or containing CLA (0.1 ml), linoleic acid (0.1 ml), or dl-a-tocopherol (lOmg). Four weeks after the first treatment, liver microsomes were prepared and subsequently subjected to oxidative stress using a non-enzymatic iron-dependent lipid peroxidation system. Microsomal lipid peroxidation was measured as thiobarbituric acid-reactive substance (TBARS) production using malondialdehyde as the standard. It was found that pretreatment of mice with CLA or dl-a-tocopherol significantly decreased TBARS formation in mouse liver microsomes (p < 0.05) (Sword, J. T. and M. W. Pariza, University of Wisconsin, unpublished data). 

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. 

---