Lipid peroxidation changes

Sigala E, Kostopanagiotou G, Andreadou I, et al. (2004) Histological and lipid peroxidation changes after administration of 2-acetylaminofluorene in a rat liver injury model following selective periportal and pericentral damage. Toxicology 196 155-163. 

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. 

Esterbauer et al. (1991) have demonstrated that /3-carotene becomes an effective antioxidant after the depletion of vitamin E. Our studies of LDL isolated from matched rheumatoid serum and synovial fluid demonstrate a depletion of /8-carotene (Section 2.2.2.2). Oncley et al. (1952) stated that the progressive changes in the absorption spectra of LDL were correlated with the autooxidation of constituent fatty acids, the auto-oxidation being the most likely cause of carotenoid degradation. The observation that /3-carotene levels in synovial fluid LDL are lower than those of matched plasma LDL (Section 2.2.2) is interesting in that /3-carotene functions as the most effective antioxidant under conditions of low fOi (Burton and Traber, 1990). As discussed above (Section 2.1.3), the rheumatoid joint is both hypoxic and acidotic. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples (Fairburn etal., 1992). This difference could not be accounted for by the lower concentrations of lipids and lipoproteins within synovial fluid. The low levels of both vitamin E and /3-carotene in rheumatoid synovial fluid are consistent with the consumption of lipid-soluble antioxidants within the arthritic joint due to their role in terminating the process of lipid peroxidation (Fairburn et al., 1992). 

Isolated hepatocytes incubated with ionic iron rapidly undergo lipid peroxidation. Some studies have not shown a consequent decrease in viability (as indicated by uptake of trypan blue or release of enzymes). This is probably a result of short incubation times, as changes in viability lag behind increases in lipid peroxidation, and may not occur for more than 2 h after lipid peroxidation begins (Bacon and Britton, 1990). Recent studies have shown strong correlations between increased lipid peroxidation [production of thiobarbituric acid (TBA) reactants] and loss of cell viability (trypan blue staining) (Bacon and Britton, 1989). The significance of the lag between lipid peroxidation and decreases in cell viability is as yet uncertain. 

Furthermore, depletion of hepatic GSH induced chemically or by fasting augmented hepatic I/R-induced enzyme release and promoted lipid peroxidation (Jennische, 1984 Stein et al., 1991) Benoit et al. (1992) have used portacaval-shunted rats as a model of chronic hepatic ischaemia, and were able to show decreases in total levels of SOD and xanthine dehydrogenase, but no significant change in catalase or glutathione peroxidase. 

Dabrowski, A., Gabryelewicz, A. and Chwiecko, M. (1991). Products of lipid peroxidation and changes in sulphydryl compounds in pancreatic tissue of rats with caerulein-induced acute pancreatitis. Biochem. Med. Metab. Biol. 46, 10-16. 

Golberg, L., Martin, L.E. and Batchelor, A. (1962). Biochemical changes in the tissues of animals injected with iron. 3. Lipid peroxidation. Biochem. J. 83, 291-298. 

Nonaka, A., Manabe, T., Tamura, K., Asano, N., Imanishi, K. and Tobe, T. (1989b). Changes of xanthine oxidase, lipid peroxide and superoxide dismutase in mouse acute pancreatitis. Digestion 43, 41-46. 

Several studies have demonstrated that treatment of diabetic patients with the sulphonylurea, gliclazide, is associated with a fall in lipid peroxidation, protein fluorescence and beneficial effects on platelet function (Florkowski et al., 1988 Jennings et al., 1992). These changes were seen to be independent of changes in giycaemic control. 

Stohs, S.J., Hassan, M.Q. and Murray, W.J. (1984). Effects of a-tocopherol and retinol acetate on TCDD-mediated changes in lipid peroxidation, glutathione peroxidase activity and survival. Xenobiotica 14, 533-537. 

Haider SS, Hasan M. 1984. Neurochemical changes by inhalation of environmental pollutants sulfur dioxide and hydrogen sulfide Degradation of total lipids, elevation of lipid peroxidation and enzyme activity in discrete regions of the guinea pig brain and spinal cord. Ind Health 22 23-31. 

In our previous research, we found that the antialgal allelochemical Ethyl 2-Methylacetoacetate (EMA) caused loss of cell membrane integrity. It hinted that EMA may cause a change in the membrane. It is reported that environmental stress may increase the concentration of ROS in plant cell. The excessive ROS may cause a decrease of antioxidation enzymes activity and lipid peroxidation. The effect of EMA on the activity of SOD and POD and lipid fatty acids of Chlorella pyrenoidosa, Chlorella vulagaris and Microcystis aeruginosa were evaluated to elucidate the mode of action of EMA. 

Wise JA, Morin RJ, Sanderson R and Blum K. (1996). Changes in plasma carotenoid, alpha-tocopherol, and lipid peroxide levels in response to supplementation with concentrated fruit and vegetable extracts a pilot study. Curr Ther Res 57(6) 445 t61. 

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