E and lipid peroxidation

Oils that have undergone lipid peroxidation may have adverse physiological effects if consumed. For example, Eder (1999) found that oxidized oils in a diet could diminish the ability of rat heart and liver tissues to desaturate fatty acids. Work by Sheehy et al in 1994 showed that the consumption of thermally oxidized sunflower oil by chicks reduces the tissue content of a-tocopherol and increases the susceptibility of tissues to lipid peroxidation. The addition of vitamin E to refined olive oil increases the stability of the oil under pro-oxidant conditions and decreases the oxidative damage caused by adriamycin in rats (Quiles et al, 1999). 

The biological membranes of subcellular organelles are primary sites for lipid peroxidation damage (Sevanian and Ursini, 2000). Lipid hydroperoxides and aldehydic lipid peroxidation can also induce strand breaks in DNA (Yang and Schaich, 1996). 4-HNE accumulates rapidly following spinal cord injury 

Diet Number of volunteers Pentane formation rate (pmol/kg-min) Plasma vitamin E (IIM) 

Lipid peroxidation is well documented in vitro but is more difficult to verify in intact organisms. The pioneering work of Lemoyne et al. (Lemoyne et al., 1988 Van Gossum et al., 1988 Lemoyne etal, 1987) demonstrated, however, that vitamin E is an effective in vivo antioxidant. Pentane is formed by the peroxidation of n-6 fatty acids and can be collected from human breath and analysed by gas chromatography. As shown in Table 5, Lemoyne et al. (1987) showed that the rate of breath pentane formation was inversely correlated with plasma vitamin E levels, and could be suppressed by taking a vitamin E supplement. 

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Minor chromosomal abnormalities Inhibition of intracellular hydrolytic enzymes of alveolar macrophages increased fraction of polymorphonuclear leukocytes Alterations in blood, including red-cell membrane and enzyme changes and increased serum vitamin E and lipid peroxides Decreased lung DNA synthesis Decreased electric response of specific areas of brain with evoked-response technique... 

Alterations in blood, induding Man red-cell membrane and enzyme diaiiges and increased serum vitamin E and lipid peroxides... 

Hepatic Effects. No studies were located regarding hepatic effects in humans after exposure to 3,3 -dichlorobenzidine. Information from animal studies on the liver effects of exposure to 3,3 -dichloro-benzidine suggests that exposme to sufficiently high levels of the compoimd could cause liver injury as indicated by modest elevation in serum transaminase activity, fatty liver (Stula et al. 1978), decrease in hepatic vitamin E, and lipid peroxidation (Iba 1987a Iba and Lang 1988 Iba and Thomas 1988). Some of these effects may contribute to the liver tumors induced. However, it is not known whether these liver injuries will occur in humans exposed to 3,3 -dichlorobenzidine at levels at which it occurs at hazardous... 

Braughler, J.M, and Hall, E.D. (1989). Central nervous system trauma and stroke. I. Biochemical considerations for oxygen radical formation and lipid peroxidation. Free Rad. Biol. Med. 6, 289-301. 

Dillard, C.J., Litov, R.E., Savin, W.M. and Tappel, A.L. (1978). Effects of exercise, vitamin E and ozone on pulmonary function and lipid peroxidation. J. Appl. Physiol. 45, 927-932. 

Normally, the cascade from oxygen to water is well controlled by SOD, catalase and endogenous antioxidants such as glutathione, ascorbate and vitamin E. Vitamin E is the most important membrane-bound antioxidant. However, during ischaemia, the local control of ROS is lost, thus reactive free radicals can attack the membranes and lipid peroxidation begins. Endogenous antioxidants can be supplemented. This section describes this supplementation strategy. 

Sawada, M., J.C. Carlson, and H.E. Enesco. 1990. The effects of UV radiation and antioxidants on life span and lipid peroxidation in the rotifer Asplanchna brightwelli. Arch. Gerontol. Geriatr. 10 27-36. 

Ramstock ER et al Trialkyl lead metabolism and lipid peroxidation in vivo in vitamin E-and selenium deficient rats as measured by ethane production. Toxicol Appl Pharmacol 54 251-257, 1980... 

Haloalkanes. Certain haloalkanes and haloalkane-containing mixtures have been demonstrated to potentiate carbon tetrachloride hepatotoxicity. Pretreatment of rats with trichloroethylene (TCE) enhanced carbon tetrachloride-induced hepatotoxicity, and a mixture of nontoxic doses of TCE and carbon tetrachloride elicited moderate to severe liver injury (Pessayre et al. 1982). The researchers believed that the interaction was mediated by TCE itself rather than its metabolites. TCE can also potentiate hepatic damage produced by low (10 ppm) concentrations of carbon tetrachloride in ethanol pretreated rats (Ikatsu and Nakajima 1992). Acetone was a more potent potentiator of carbon tetrachloride hepatotoxicity than was TCE, and acetone pretreatment also enhanced the hepatotoxic response of rats to a TCE-carbon tetrachloride mixture (Charbonneau et al. 1986). The potentiating action of acetone may involve not only increased metabolic activation of TCE and/or carbon tetrachloride, but also possible alteration of the integrity of organelle membranes. Carbon tetrachloride-induced liver necrosis and lipid peroxidation in the rat has been reported to be potentiated by 1,2- dichloroethane in an interaction that does not involve depletion of reduced liver glutathione, and that is prevented by vitamin E (Aragno et al. 1992). 

Moen, M. A. Hammel, K. E. (1994). Lipid peroxidation by the manganese peroxidase of Phanerochaete chrysosporium is the basis for phenanthrene oxidation by the intact fungus. Applied and Environmental Microbiology, 60, 1956-61. 

Pepicelli O., Fedele E., Berardi M., Raiteri M., Levi G., Greco A., Ajmone-Cat M. A., and Minghetti L. (2005). Cyclo-oxygenase-1 and -2 differently contribute to prostaglandin E2 synthesis and lipid peroxidation after in vivo activation of N-methyl-D-aspartate receptors in rat hippocampus. J. Neurochem. 93 1561-1567. 

FIGURE 29.1 Pathways of the chain-breaking action of vitamin E in lipid peroxidation and its subsequent regeneration. LOOH lipid hydroperoxide, LOO lipid peroxyl radical, vitamin C ascorbate radical (semi-dehydroascorbate), vitamin E a-tocopheroxyl radical. The lipid peroxyl radical is reduced to lipid hydroperoxide by tocopherol. The resulting tocopheroxyl radical can be re-reduced by ascorbate. The thus formed ascorbate radical can be reduced to ascorbate by the NADH-dependent semidehydroascorbate reductase. 

T. Yokozawa, H. Y. Kim, and E. J. Cho, Erythritol attenuates the diabetic oxidative stress through modulating glucose metabolism and lipid peroxidation in streptozotocin-induced diabetic rats, J. Agric. Food Chem., 2002, 50, 5485-5489. 

Farombi, E.O., Tahnteng, J.C., Agboola, A.O., Nwankwo, J.O. and Emerole, C.O. (2000) Chemoprevention of 2-acetylaminofluorene-induced hepatotoxicity and lipid peroxidation in rats by kolaviron-A Garcinia kola seed extract. Food and Chemical Toxicology 38(6), 535-541. 

There are few reports on the inhibitory effect of conjugated polyenes on the growth of cancer cell lines. Begin et al. (1988) reported the toxic effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on several kinds of tumor cells other polyunsaturated fatty acids, i.e., arachidonic acid (22 4n-6), a-linolenic acid (18 3n-3), and y-linolenic acid (18 3n-6) have cytotoxic action on several tumor cell lines at concentrations above 50 pM. Further, Tsuzuki et al. (2004) demonstrated that the anticarcinogenic effect of CLN are directly associated with lipid peroxidation. They transplanted human colon cancer cells (DLD-1) into nude mice, and CLA (9c, lit and lOt, 12c-18 2) and CLN (9c, lit, 13t-18 3) were administered to animals. Tumor growth was suppressed by the supplementation of CLA and CLN, and the extent of suppression was CLN >9c, llt-CLA.>10t, 12c-CLA, in that order. Furthermore, DNA fragmentation was enhanced and lipid peroxidation increased in tumor cells of the CLN-fed mouse. Thus this study indicates the possibility of seaweeds as potential sources of anticancer substances. 

High-dose pretreatment with vitamin E (1000IU p.o. once daily for 5 days) has been shown to promote the chronic recovery of spinal-cord injured cats [45]. This is consistent with its ability to prevent post-traumatic spinal-cord hypoperfusion [29] and lipid peroxidation [8] and with the hypothesis that oxygen-radical generation and lipid peroxidation are important mediators of post-traumatic spinal-cord pathophysiology and degeneration. 

Microinjection of ferrous iron (i.e. ferrous chloride) has also been shown to produce focal edema in rat brain, the degree of which is correlated with tissue levels of the lipid-peroxidation product malonyldialdehyde. Pretreatment with vitamin E (600 mg/kg intramuscularly once daily for 5 days) together with selenium (5 ppm in the drinking water) reduced the iron-induced edema and lipid peroxidation [54]. Similarly, the 21-aminosteroid U-74006F can also reduce iron-induced opening of the blood-brain barrier [53],... 

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