Damage by Lipid Peroxidation

Subcell ular particle Evidence for lipid peroxidation Damage by in vitro Metabolic derangements in vivo which could result from peroxidation 

Liver mitochondria of vitamin E-deficient rabbit Increased TBA reactants Increased TBA, absorption 0, Severe destruction of enzymes and cytochromes of electron transport Uncoupling of oxidative phos-phorydation metabolic declinei swelling of mitochondria 

Lj sosomes Cooxidation by per-oxidizing lipid Breaking of membrane and release of hydrolytic enzymes Some of the catabolic reactions of muscular dystrophy involving protein, nucleic acid, and mucopolysaccharide hydrolysis 

Erythrocytes of vitamin E-deficient rats None Increased TBA by Oj or dialuric acid Hemolysis Decreased erythrocyte lifetime and anemia 

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Moreover, under certain conditions these phenolic compounds could also act as pro-oxidants. In the presence of redox-active metal ions such as Cu or Fe, phenolic compounds react with O2 to generate phenoxyl radicals. Under normal growth conditions phenoxyl radicals can be rapidly deactivated by polymerization or enzymatic reduction. However, if the phenoxyl radical concentrations are too high and/or the lifetime is increased, they could initiate DNA damage or lipid peroxidation and exhibit cytotoxicities. Curcumin, demethoxycurcumin, and bisdemethoxycurcumin have been reported to induce... 

Ueda K, Kobayashi S, Morita J, KomanoT (1985) Site-specific DNA damage caused by lipid peroxidation products. Biochim Biophys Acta 824 341-348... 

There is considerable debate concerning the role played by free radical reactions, protein oxidation, DNA damage and lipid peroxidation in human disease and toxicology. Radical species have indeed been implicated in many disease states (Table 2.1). The question as to whether free radicals are a major cause of tissue damage in human disease or an accompaniment to or a consequence of such injury is by no means clear in many instances. However, what is clear is that diseased or damaged tissues undergo radical reactions more readily than normal, which may exacerbate the primary lesion. 

A. Dupin et al.. Protection by carnosine of calcium transport from damage induced by lipid peroxidation. Bull. Exp. Biol. Med. (Russian), 97 (1984) 186-188. 

Antioxidant activity by reduction of oxidative DNA damage and lipid peroxidation, and ability to quench free radicals 103... 

C. In animal models of intoxication, damage is most severe in areas of the brain that are highly sensitive to ischemia and often correlates with the severity of systemic hypotension. Postanoxic injury appears to be complicated by lipid peroxidation, excessive release of excitatory neurotransmitters, and inflammatory changes, including adherence of neutrophils to cerebral vessels. 

Lipid peroxidation, the oxidative degradation of polyunsaturated fatty acids, is implicated in several pathological conditions—ageing, hepatotoxicity, haemolysis, cancer, atherosclerosis, tumour promotion and inflammation. Selected flavonoids may exert protective effects against cell damage produced by lipid peroxidation stimulated by a variety of toxins, owing to the antioxidant properties of the compounds (Pathak et al. 1991). 

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