Melatonin reduces mortality and oxidatively mediated hepatic and renal damage due to diquat treatment (original) (raw)
Pathological aspects of lipid peroxidation
Free Radical Research, 2010
Lipid peroxidation (LPO) product accumulation in human tissues is a major cause of tissular and cellular dysfunction that plays a major role in ageing and most age-related and oxidative stress-related diseases. The current evidence for the implication of LPO in pathological processes is discussed in this review. New data and literature review are provided evaluating the role of LPO in the pathophysiology of ageing and classically oxidative stress-linked diseases, such as neurodegenerative diseases, diabetes and atherosclerosis (the main cause of cardiovascular complications). Striking evidences implicating LPO in foetal vascular dysfunction occurring in pre-eclampsia, in renal and liver diseases, as well as their role as cause and consequence to cancer development are addressed.
The pathophysiological significance of lipid peroxidation in oxidative cell injury
Hepatology, 1987
Although the complex processes which accompany oxidative stress result in damage to many cell components, peroxidative decomposition of membrane lipids and the associated changes in bulk membrane properties have frequently been considered as the basis of cell injury. This study was supported by NIH Grants HL-30286 and GM-36538.
HNE and Further Lipid Peroxidation Products
BioFactors, 2005
Oxygen free radicals are implicated in many diseases and "normal" processes, such as ischemiareperfusion injury (see myocardial infarction and stroke), cataracts, age-related macula degeneration, cancer, inflammation, aging, diabetes, and neurodegenerative diseases. Assessment of oxidative stress by measurement of lipid peroxidation (LPO) products is of biological and clinical importance when considering the multiple functions of lipids such as steroid hormones, retinoic acids, and prostaglandins. Beyond, LPO products such as 4-hydroxynonenal (HNE), acrolein, F2-isoprostanes, and oxysterols exert signal functions that significantly influence gene expression and protein synthesis, and such regulatory phenomena may affect the organism more dramatically. In short, LPO is biologically and medically important. When establishing methods for LPO measurement, one has to take into account which phase of LPO, its initiation, propagation, or termination, is to be characterized. If unstable carbon radicals are formed from fatty acids, conjugated dienes as next group of intermediates are generated by molecular rearrangement. By oxygen uptake then peroxyl radicals and, by hydrogen abstraction, lipid hydroperoxides are formed. These primary oxidation products generate secondary LPO products, such as malondialdehyde (MDA), HNE, and other aldehydes, short-chain alkanes, isoprostanes etc. Analyzing LPO therefore means either to determine the formation of oxidized products (e.g. short-chain alkanes, aldehydic LPO products, F2-isoprostanes, or oxysterols) or to monitor the loss of regular cellular constituents (substrate loss; compounds which get used up during oxidative stress, e.g. PUFA), and each approach will answer distinct questions only. Groups of analytically accessible LPO intermediates and products, which are also found in biological systems, are compiled in Fig. 1.