The peroxidation of membrane lipids by free radicals is a well-controlled, ongoing process that occurs with normal cell turnover and the normal aging process. There is also the uncontrolled process of free radical production and increased lipid peroxidation that is associated with hepatic injury as a consequence of exposure to halogenated hydrocarbons, excessive alcohol abuse, and acute or chronic iron overload. Excess free radical production and lipid peroxidation is thought to be an etiological factor in such diseases as atherosclerosis, diabetes, genetic hemochromatosis, cancer and neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease.
4-Hydroxynonenal (HNE) is a highly reactive, cytotoxic aldehyde that is released during the oxidation of o-6-unsaturated fatty acids. HNE can efficiently react with sulfhydryl groups or histidine and lysine groups of proteins to form stable HNE-protein adducts, in addition to phospholipids and nucleic acids. It is through this HNE-modification of biomolecules that HNE is thought to exert its cytotoxic effects. This multifunctional molecule may be considered as a “second toxic messenger,” which disseminates and augments initial free radical events. It is believed to be largely responsible for the cytopathological effects observed during oxidative stress. High levels of 4-HNE have been detected in a large number of disease states, indicating some involvement of this aldehyde in their pathogenesis. Some of the prominent pathobiochemical effects of 4-HNE are its stimulation of fibrogenesis and inflammation, thus indicating a potential contribution to the pathogenesis of several chronic diseases, the progression of which is supported by inflammatory reactions and characterized by fibrosis. 4-HNE may also play a role in carcinogenesis due to its ability to modulate cell proliferation through interference with the activity of cyclins and protein kinases and with the apoptotic response.
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