markers of lipidperoxidationprocesses was determined following AOAC (1984) , analysis method no. 28.054. In addition, amounts of malondialdehyde (MDA), a meta-stable end product of lipidperoxidationprocesses, was determined based on the procedure of
This study was designed to investigate the effects of excess (24.5 mg Se/kg feed) inorganic and organic dietary selenium supplementation on 3-week-old broilers. The experiments lasted 4 days. Intensity of lipid peroxidation processes (malondialdehyde, MDA) and the amount (reduced glutathione, GSH) and activity (glutathione peroxidase activity, GSHPx) of gluathione redox system were measured in blood plasma, red blood cell hemolysate and liver: Voluntary feed intake in the selenium-treated groups reduced remarkably. Elevated GSH concentration and GSHPx activity were measured in plasma and liver of both selenium-treated groups compared to the untreated control and the ‘pair-fed’ controls. The lipid peroxidation processes in the liver showed higher intensity than the control due to both selenium treatment. The applied dose of selenite and selenomethionine does not inhibit, but even improves the activity of glutathione redox system in the liver during the early period of selenium exposure.
Lipid peroxidation is generally thought to be a major mechanism of cell injury in aerobic organisms subjected to oxidative stress. All cellular membranes are especially vulnerable to oxidation due to their high concentration of polyunsaturated fatty acids. However, birds have special adaptations for preventing membrane damage caused by reactive oxygen species. This study examines fatty acid profiles and susceptibility to lipid peroxidation in liver and heart mitochondria obtained from Adelie penguin
. The saturated fatty acids in these organelles represent approximately 40–50% of total fatty acids whereas the polyunsaturated fatty acid composition was highly distinctive, characterized by almost equal amounts of 18:2 n-6; 20:4n-6 and 22:6 n-3 in liver mitochondria, and a higher proportion of 18:2 n-6 compared to 20:4n-6 and 22:6 n-3 in heart mitochondria. The concentration of total unsaturated fatty acids of liver and heart mitochondria was approximately 50% and 60%, respectively, with a prevalence of oleic acid C18:1 n9. The rate C20:4 n6 / C18:2 n6 and the unsaturation index was similar in liver and heart mitochondria; 104.33 ± 6.73 and 100.09 ± 3.07, respectively. Light emission originating from these organelles showed no statistically significant differences and the polyunsaturated fatty acid profiles did not change during the lipid peroxidation process.
An experimental surgical model was developed in rats after a short term alimentary induced hyperlipidemy to study the direct effect of bile on the colonic mucosa, with regard to the cancerogenic properties of lipid rich diet. The purpose of this study was to light on the role of fatty acid alteration and lipid peroxidation processes of bile in the epithelial cell damage. Animals were fed with normal (group A) and fat rich diet (group B) for 10 days and then bile samples were collected by the cannulation of the common bile duct in deep anaesthesia. The circulation preserved colons of control rats were treated either with bile from the control or hyperlipidemic rats. The treatment was carried out for 30 minutes. The electronmicroscopic alterations of epithelial cells (both enterocytes and goblet cells) caused by bile from hyperlipidemic rats were significantly greater than that of controls. Unfavourable changes of the redox state of the colonic mucosa were also detected both in the hyperlipidemic and bile treated groups. A significant increase was observed in the free-SH concentration of the two bile treated groups against the untreated animals. The changes could be explained among others by the modified bile fatty acid composition. The present study supports that the alimentary modified bile can influence the structure of the epithelium of colonic mucosa and it can be one of the inducing factor of carcinogenesis.
termination marker of lipidperoxidationprocesses, TBARS expressed as MDA, was significantly lower in the blood plasma on day 7 but significantly higher on days 14 and 21 of AFB 1 treatment as compared to the control. On the 21st day of exposure, the MDA
]. It has been known that exercise-induced membrane damage might be related to free radical mediated lipid peroxidation, and serum MDA is one of the byproducts in the lipidperoxidationprocess that has been used as a marker of oxidative stress [ 29
creating a vicious circle [ 39 ]. ROS drive a lipidperoxidationprocess that culminates in the generation of toxic aldehydes (e.g. MDA). Besides mitochondrial damage, they are thought to cause abnormalities in meiotic division and oocyte maturation