Plasma lipid peroxidation

Kim, H.S. and Lee, B.M., Protective effects of antioxidant supplementation on plasma lipid peroxidation in smokers, J. Toxicol. Environ. Health A, 63, 583, 2001. Gaziano, J.M. et al.. Supplementation with beta-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation. Atherosclerosis, 112, 187, 1995. Sutherland, W.H.F. et al.. Supplementation with tomato juice increases plasma lycopene but does not alter susceptibility to oxidation of low-density lipoproteins from renal transplant recipients, Clin. Nephrol, 52, 30, 1999. 

Lemonnier, P., Cresteil, D., Feneant, M., Couturier, M., Bernard, O. and AlagjUe, D. (1987). Plasma lipid peroxides in cholestatic children. Acta Paediatr. Scand. 76, 928-934. 

Table 12.1 Studies of serum/plasma lipid peroxides in human diabetes modified from Lyons (1991)...

Other examples of possible damaging effects of radio frequency MFs on humans are the MF effects on cellular phones. Moustafa et al. [216] suggested that acute exposure to the MFs of commercially available cellular phones for 1, 2, or 4 h significantly increased plasma lipid peroxidation and decreased the activities of SOD and glutathione peroxidase in erythrocytes. 

The efficiency of vitamin E in the suppression of free radical-mediated damage induced by iron overload has been studied in animals and humans. Galleano and Puntarulo [46] showed that iron overload increased lipid and protein peroxidation in rat liver. Vitamin E supplementation successfully suppressed these effects and led to an increase in a-tocopherol, ubiquinone-9, and ubiquinone-10 contents in liver. Important results were obtained by Roob et al. [47] who found that vitamin E supplementation attenuated lipid peroxidation (measured as plasma MDA and plasma lipid peroxides) in patients on hemodialysis after receiving iron hydroxide sucrose complex intravenously during hemodialysis session. These findings support the proposal that iron overload enhances free radical-mediated damage in humans. 

Oral vitamin E, 300 mg and 600 mg daily for 2 weeks, administered to type II and IV hyperlipoproteinaemia patients increased the serum vitamin E concentration 2- fold and suppressed the normally elevated plasma lipid peroxide... 

Rigas, J.R., Warrell, R.P., Jr., and Young, C.W. 1994. Elevated plasma lipid peroxide content correlates with rapid plasma clearance of all-trans-retinoic acid in patients with advanced cancer. 

Gradual decreasing of the PJ dosage in these three subjects down to 40 mL/day for 1 week, and then to 20 mL/day for an additional 2 weeks, did not significantly affect plasma lipid peroxidation, which remained low in comparison to the levels obtained after supplementation of 80 mL of PJ concentrate/day. Two weeks after... 

The effect of PJ consumption by patients with CAS on their serum oxidative state was measured also as serum concentration of antibodies against Ox-LDL.31 A significant (p < 0.01) reduction in the concentration of antibodies against Ox-LDL by 24 and 19% was observed after 1 and 3 months of PJ consumption, respectively (from 2070 61 EU/mL before treatment to 1563 69 and 1670 52 F.lI/mL after 1 and 3 months of PJ consumption, respectively). Total antioxidant status (TAS) in serum from these patients was substantially increased by 2.3-fold (from 0.95 0.12 nmol/L at baseline up to 2.20 0.25 nmol/L after 12 months of PJ consumption). These results indicate that PJ administration to patients with CAS substantially reduced their serum oxidative status and could thus inhibit plasma lipid peroxidation. The susceptibility of the patient s plasma to free radical-induced oxidation decreased after 12 months of PJ consumption by 62% (from 209 18 at baseline to 79 6 nmol of peroxides/milliliter). The effect of PJ consumption on serum oxidative state was recently measured also in patients with non-insulin-dependent diabetes mellitus (NIDDM). Consumption of 50 mL of PJ per day for a period of 3 months resulted in a significant reduction in serum lipid peroxides and thiobarbituric acid reactive substance (TBAR) levels by 56 and 28%, respectively.32... 

PJ consumption exhibited antioxidative effects also when administered to E° mice.28 The basal oxidative state, measured as lipid peroxides in plasma of control E° mice (that did not consume PJ), increased gradually during aging from 260 nmol/mL of plasma at 6 weeks of age to 309 and 535 nmol/mL of plasma after 9 and 14 weeks of age, respectively. Following PJ consumption, plasma lipid peroxidation was markedly reduced, and this effect was PJ concentration dependent (Figure 8.3B). Similarly, serum total antioxidant status was higher in E° mice that consumed PJ in comparison to control mice, and this effect was again juice concentration dependent.28... 

Skibska, B., Jozefowicz-Okonkwo, G., and Goraca, A. 2006. Protective effects of early administration of alpha-lipoic acid against lipopolysaccharide-induced plasma lipid peroxidation. Pharmacol. Rep. 58 399-404. 

MahadikSP, MukherjeeS, Scheffer R, CorrentiEE, Mahadik JS. 1998. Elevated plasma lipid peroxides at the onset of nonaffective psychosis. Biol Psychiatry 43 674-679. Malaspina D, Coleman E, Goetz RR, Harkavy-Friedman J, Corcoran C, et al. 2002. Odor identification, eye tracking and deficit syndrome schizophrenia. Biol Psychiatry 51 809-815. 

Although the basic pathogenesis of diabetes is not well understood, there is increasing evidence that free radicals are involved. For example, early studies showed that plasma lipid peroxide levels are consistently elevated in diabetic compared with nondiabetic (N9, S5) patients with NIDDM also have higher levels of plasma TBARS and conjugated dienes than normal (Cl5). In addition, NIDDM patients with retinopathy have increased plasma levels of TBARS (Ul). Moreover, neutrophils from diabetics contain significantly higher levels of Oj due to their decreased SOD activity (N4). Numerous other studies have been published on this topic, and it has been recently reviewed (K15). 

Without ceruloplasmin activity the ferrous iron is taken up by brain cells leading to iron overload and cell death. A similar situation occurs in peripheral tissues. This is supported by studies indicating a significant increase in plasma lipid peroxidation in patients with aceruloplasminemia. ... 

Kamal AA, Gomaa A, El Khafif M, et al. 1989. Plasma lipid peroxides among workers exposed to silica or asbestos dusts. Environ Res 49 173-180. 

Mahadik SP, Mukheijee S, Scheffer R, Correnti EE, Mahadik JS. Elevated plasma lipid peroxides at the onset of nonaffective psychosis. Biol Psychiahy 1998 43 674-679... 

Since high plasma cholesterol levels and plasma lipid peroxidation are associated with arteriosclerosis, Aviram et al.175 studied the effect of high... 

Aviram, M., Cogan, U., and Mokady, S., Excessive dietary tryptophan enhances plasma lipid peroxidation in rats, 88, 29, 1991. 

Hutchins, A.M. I.E. Mclver C.S. Johnston. Soy isoflavone and ascorbic acid supplementation alone or in combination minimally affect plasma lipid peroxides in healthy postmenopausal women./. Am. Diet. Assoc. 2005, 105, 1134-1137. 

Although increased levels of lipid peroxidation endproducts are found in most human diseases, the occurrence of lipid peroxidation does not always imply a state of disease. For example, increased levels of lipid peroxidation also occur in fasting human subjects, by the breakdown of fat (65). A certain level of lipid peroxidation may actually be expected after exposure to CIA, as most polyunsaturated fatty acids are more susceptible to the attack of oxygen radicals than monounsaturated fatty acids or saturated fatty acids (66). For example, supplementation with fish oil significantly increased plasma lipid peroxides in women (67, 68). Work by Banni et al. showed that CLA does not behave differently under oxidative stress than regular polyunsaturated fatty acids (51). The control oil used in the studies by Riserus et al. (35) and Basu et al. (64) was olive oil, which contains high levels of the monounsaturated acid oleic acid and has been shown to work as an anti-oxidant (69). 

A. Dietrich-Muszalska, B. Olas, B. Kontek, J. Rabe-Jablonska, Beta-glucan from Saccharomyces cerevisiae reduces plasma lipid peroxidation induced by haloperidol, Int. J. Biol Macromol, 49,113-116, 2011. 

The flavanol catechin prevented plasma lipid peroxidation that was induced by azo compounds such as the water-soluble 2,2-azobis, 2-amidinopropane hydrochloride (AAPH) or the lipid-soluble 2,2-azobis, 2,4-dimethylvaleronitrile... 

Aortic atherosclerotic lesion areas were reduced in mice that consumed 1.52 mg of rosmarinic acid /kg/day compared to mice on the control diet. Figure 3 shows the photomicrographs of typical atherosclerotic lesion of the aortic arch of apolipoprotein E-deficient mice after treatment. Rosmarinic acid inhibited plasma lipid peroxide levels in apolipoprotein E-deficient mice without affecting the total cholesterol levels in plasma, indicating that the anti-atherosclerotic properties of rosmarinic acid may be due, in part, to its antioxidative action which inhibits the increase in lipid peroxides. 

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