Homeostasis between lipid peroxidation and antioxidant enzyme activities in healthy human aging

Rodríguez-Martínez, María; Ruíz-Torres, A

doi:10.1016/0047-6374(92)90137-3

Cited by 86 publications

(49 citation statements)

References 15 publications

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“…Both overall and abdominal obesity 16 have been said to increase LDL oxidizability. In addition, age may 17 or may not 18 have this same effect. Consequently, we performed multiple regression analysis to determine whether any of these factors could affect LDL oxidation status independently of insulin resistance or its metabolic covariates.…”

Section: Resultsmentioning

confidence: 99%

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

Carantoni

Abbasi

Warmerdam

et al. 1998

ATVB

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Abstract-This study was performed in 36 healthy volunteers to define the relationship between plasma concentrations of partially oxidized low density lipoprotein (poxLDL), plasma glucose and insulin responses to oral glucose, and steady-state plasma glucose (SSPG) concentrations after a 180-minute infusion of somatostatin, insulin, and glucose. The concentration of poxLDL was estimated by determining the amount of conjugated dienes formed during in vitro LDL oxidation in the presence or absence of alanine. Under these conditions, the greater the in vitro antioxidant effect of alanine, the lower the amount of poxLDL that was present in plasma. Key Words: oxidized LDL Ⅲ insulin resistance Ⅲ cardiovascular disease risk factors P revious reports from our laboratory have emphasized the potential link between insulin resistance, a cluster of associated abnormalities, and atherosclerosis in nondiabetic subjects.1,2 An important component of the metabolic abnormalities associated with insulin resistance is a change in LDL particle diameter, leading to the presence of smaller and denser LDL particles.3 Given the fact that such particles are more easily oxidized, 4 it seemed to be of great interest to know whether there were any associations between insulin resistance and the oxidative states of circulating LDL. Approaching this problem is complicated by the fact that oxLDL has been detected in the arterial wall, but not in the circulation.5 LDL oxidation has usually been assessed by determining the formation of thiobarbituric acid-reactive compounds or by the lag time for conjugated-diene formation during copper oxidation-methods that do not permit determination of the oxidized state of LDL present in the circulation. 6 In an effort to overcome this problem, Picard et al 7 have described a sensitive and reproducible method to quantify the oxidized state of LDL present in the circulation on the basis of the antioxidant properties of alanine. This effect of alanine depends on the amount of peroxides present in LDL and the fact that the greater the amount of peroxides in LDL, the less the antioxidant effect of alanine. Thus, by quantifying the antioxidant effect of alanine on isolated LDL, it is possible to gain an estimate of the amount of poxLDL that is present in the circulation. Picard et al 7 used this method to show that LDL oxidation was increased in patients with type 2 diabetes who had evidence of atherosclerosis but absent in diabetic subjects with no apparent vascular disease. Since there is increasing evidence 1,2,8 that insulin resistance or compensatory hyperinsulinemia is associated with a variety of CHD risk factors, we initiated the current study to see whether there was any relationship between the resistance of insulinmediated glucose disposal or the metabolic variables associated with insulin resistance and the amount of poxLDL in nondiabetic volunteers, all of whom were in general good health. MethodsThe study population consisted of 36 healthy volunteers, 14 men and 22 women, who responded to a newspap...

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Section: Resultsmentioning

confidence: 99%

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

Carantoni

Abbasi

Warmerdam

et al. 1998

ATVB

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“…Inhibition of plasma lipid peroxidation in blood plasma was determined according to the method developed by Rodriguez-Martinez and Ruiz-Torres (1992). Plasma (400 µL), 100 µL of FeSO 4 .7H 2 O solution (500 µM), 100 µL of H 2 O 2 (500 µM), and 200 µL of Fe@Au nanospheres (2 mg/mL) were mixed and incubated for 12 h at 37 °C.…”

Section: Inhibition Of Plasma Lipid Peroxidationmentioning

confidence: 99%

“…The mixture was stirred vigorously, kept at 95 °C for 30 min, and then cooled. Following that process, 1-butanol was added to the mixture at a 1:1 ratio and the absorbance was measured at 532 nm (Rodriguez-Martinez and Ruiz-Torres, 1992 …”

Section: Inhibition Of Plasma Lipid Peroxidationmentioning

confidence: 99%

The comparison of antioxidant capacity and cytotoxic, anticarcinogenic,and genotoxic effects of Fe@Au nanosphere magnetic nanoparticles

Yegenoglu¹,

Aslım²,

Güven³

et al. 2017

Turk J Biol

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Magnetic gold nanoparticles are used in various biomedical, biochemistry, and biotechnology applications due to their controllable size distribution, long-term stability, reduced toxicity, and biocompatibility. Different coating materials, such as proteins, carbohydrates, lipids, and polyphenols, are applied to enhance the biocompatibility of nanoparticles. In this study, the effects of surface coatings of core-shell structured Fe@Au nanosphere magnetic nanoparticles with regard to antioxidant capacity and cytotoxic, anticarcinogenic, and genotoxic properties were investigated. The obtained results demonstrated that avidin-coated Fe@Au nanospheres had higher antioxidant capacities than uncoated nanospheres. Neither avidin-coated nor uncoated nanoparticles had a cytotoxic effect on normal cells (human gingival fibroblast cell line, HGF-1). In addition, they had anticarcinogenic effects on human cervical carcinoma (HeLa), human breast adenocarcinoma (MCF-7), and human colorectal adenocarcinoma (CCL-221). The genotoxic effects of nanoparticles were also evaluated with DNA tail damage ratio.

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“…MDA has also been extensively used as a marker of lipid peroxi dation mainly in processes associated with oxidative stress and vascular injury. Thus, high levels of MDA have been detected in plasma or vascular tissue in either aging [3,13,14] or diseases associated with vascular damage [15], such as diabetes [16][17][18], hypertension [20,21], or atherosclerosis [22,23], A common finding in these dis eases, as well as in aging, is the impairment of endothe lium-dependent relaxations, especially those evoked by acetylcholine (ACh) [24][25][26][27][28], Despite these data, there are no studies, to our knowledge, that analyze whether MDA may interfere with endothelium-dependent relaxations. If this occurs it could justify, at least in part, the reduction of these relaxations in the above-mentioned processes.…”

Section: Introductionmentioning

confidence: 99%

“…Lipid peroxidation and peroxidation products are the focus of intense current interest in biomedical and phar macological research since they play an important role in the pathogenesis of several clinically significant diseases [1,2], as well as in the physiological changes associated with aging process [3], Lipid peroxidation may be pro duced: (a) in a nonenzymatic manner, in which polyunsat urated fatty acids (PUFA) oxygenation can be induced by oxygen-derived free radicals and transition metals [4,5], and (b) in an enzymatic manner, in which PUFA oxygen ation leads to synthesis of the collectively termed eicosanoids [6,7], Malondialdehyde (MDA) is formed as a product of either the nonenzymatic lipid oxidation or enzymatic arachidonic acid oxygenation in the cyclooxy genase pathway [8], Thus, thromboxane synthase con verts prostaglandin H2 into thromboxane A2, heptadecatrienoic acid and MDA in equimolar amounts [9].…”

Section: Introductionmentioning

confidence: 99%

Impairment of Acetylcholine Relaxations by Malondialdehyde, a Marker of Lipid Peroxidation

Rodríguez-Martínez

Martı́nez-Orgado²,

Salaíces³

et al. 1996

J Vasc Res

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The effect of malondialdehyde (MDA), a lipid peroxidation marker, on the relaxations evoked by acetylcholine (ACh) was analyzed in tail arteries of Sprague-Dawley rats, which have MDA plasma levels of 0.43 ± 0.10 µM. MDA (0.5–30 µM) produced an inhibition of ACh relaxations that persisted after repeated washing periods, and was independent of the incubation time. MDA did not modify the vasodilator responses to either exogenous nitric oxide (NO) or sodium nitroprusside, a NO donor. L-Arginine (the NO synthase substrate) did not prevent the impairment of relaxations to ACh caused by MDA. The association of N^ω-nitro-L-arginine methyl ester (a NO synthase inhibitor) and MDA produced an additive inhibition of the Ach induced relaxations. Superoxide dismutase (a superoxide anion scavenger) completely reversed the inhibitory effect of MDA. These results suggest: (1) MDA is not only a marker of lipid peroxidation but also an agent that can impair endothelium-dependent relaxations; (2) this impairment does not seem to be due to an interference with guanylate cyclase activation by NO or with NO synthase pathway; (3) the effect of MDA appears to be mediated by superoxide anion, and (4) MDA could propagate lipid peroxidation chain reactions in endothelial membranes, that could alter the function of muscarinic receptors.

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Homeostasis between lipid peroxidation and antioxidant enzyme activities in healthy human aging

Cited by 86 publications

References 15 publications

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

The comparison of antioxidant capacity and cytotoxic, anticarcinogenic,and genotoxic effects of Fe@Au nanosphere magnetic nanoparticles

Impairment of Acetylcholine Relaxations by Malondialdehyde, a Marker of Lipid Peroxidation

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