Induced expression of manganese superoxide dismutase by non-toxic concentrations of oxidized low-density lipoprotein (oxLDL) protects against oxLDL-mediated cytotoxicity

Shatrov, V A; Brüne, Bernhard

doi:10.1042/bj20030420

Cited by 31 publications

(15 citation statements)

References 47 publications

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“…Many investigations indicated that MnSOD may play roles to protect against atherosclerosis and plaque formation. MnSOD is reported to inhibit the oxidation of low density lipid and protect against endothelial dysfunction [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Chromium and Manganese Levels in Biological Samples of Pakistani Myocardial Infarction Patients at Different Stages as Related to Controls

Afridi

Kazi

et al. 2010

Biol Trace Elem Res

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It has been speculated that trace elements may play a role in the pathogenesis of heart diseases In the present study, we aimed to access the levels of chromium (Cr) and manganese (Mn) in biological samples (whole blood, urine, and scalp hair) of myocardial infarction (MI) patients of both gender age ranged (45-60 years) at first, second, and third heart attack (n = 130), hospitalized in cardiac ward of National Hospital of Hyderabad city (Pakistan). For comparison, healthy age-matched referent subjects (n = 61), of both gender were also selected. The Cr and Mn in biological samples were measured by electrothermal atomic absorption spectrometry, prior to microwave-assisted acid digestion. The validity of the methodology was checked by the biological certified reference materials. During this study, 78% of 32 registered patients of third MI attack (aged >50 years) were died. In these subjects the concentration of Cr and Mn were decreased by 24.7% and 19.8% in scalp hair, while in blood samples 17.9% and 12.4%, respectively, as compared to those who tolerated third MI attack (p = 0.063). Although these data do not prove a causal relationship, these results are consistent with the hypothesis that heart disease may cause deficiencies of certain essential trace elements. The excretion levels of Cr and Mn in urine samples of first MCI were higher than controls at p values (0.029 and 0.011), respectively, whereas the excretion rates of both elements were further enhance after second myocardial infarction attack. The Cr and Mn concentration was inversely associated with the risk of myocardial infarction attacks in both genders. These results add to an increasing body of evidence that, Cr and Mn are importance for cardiovascular health.

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Section: Introductionmentioning

confidence: 99%

Chromium and Manganese Levels in Biological Samples of Pakistani Myocardial Infarction Patients at Different Stages as Related to Controls

Afridi

Kazi

et al. 2010

Biol Trace Elem Res

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“…In contrast, oxLDL can also contribute to the adaptive antiatherogenic responses of endothelium through the transcriptional regulation of antioxidant enzymes (2,23,36). Mitochondrial involvement is implied from the finding that nontoxic concentrations of oxLDL lead to induction of manganese superoxide dismutase and complex I (9,50). Many of these responses can be recapitulated using defined lipid oxidation products such as the electrophilic cyclopentenones (25,33).…”

mentioning

confidence: 88%

Oxidized LDL induces mitochondrially associated reactive oxygen/nitrogen species formation in endothelial cells

Żmijewski

Moellering

Goffe

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

128

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Exposure of cells to complex mixtures of oxidized lipids such as those found in oxidized low-density lipoprotein (oxLDL) induce reactive oxygen and nitrogen species (ROS/RNS) formation. The source of the ROS/RNS within cells is unknown; it is thought they may be involved in redox cell signaling. Although this possibility was initially overlooked, it is becoming clear that mitochondria, which are a source of superoxide and hydrogen peroxide, may play a critical role in the response of cells on exposure to oxidized lipids. In this study, we tested the possibility that mitochondria are a potential source of oxLDL-dependent formation of ROS/RNS in endothelial cells. Using confocal microscopy, we demonstrated that a significant proportion of oxLDL-dependent dichlorodihydrofluorescein (DCF) fluorescence is colocalized to mitochondria. In support of this concept, rho0 endothelial cells showed a substantial decrease in ROS/RNS formation stimulated by oxLDL. In contrast, mostly nonmitochondrial DCF fluorescence was detected in cells exposed to an extracellular source of hydrogen peroxide. The exposure of cells to a nitric oxide synthase inhibitor and urate resulted in a decrease in oxLDL-induced DCF fluorescence that was restored by addition of nitric oxide donors to the medium. Taken together, these results suggest that oxLDL-dependent DCF fluorescence is mitochondrially associated and may be due to the formation of peroxynitrite.

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“…50 SOD2 is inactivated by ONOO − 51 and its activity is decreased with age 52 . Expression of SOD2 is upregulated by various cytokines and agonists in a redox-dependent manner 53 . SOD2 overexpression attenuates H 2 O 2 -induced apoptosis, 54 decreases lipid peroxidation and reduces the age-related decline in mitochondrial ATP.…”

Section: Mitochondrial Function and Production Of Mitochondrial Rosmentioning

confidence: 99%

Cross talk between mitochondria and NADPH oxidases

Dikalov

2011

Free Radical Biology and Medicine

701

537

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Reactive oxygen species (ROS) play an important role in physiological and pathological processes. In recent years, a feed-forward regulation of the ROS sources has been reported. The interaction between main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. This work summarizes the latest findings on the role of crosstalk between mitochondria and NADPH oxidases in pathophysiological processes. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain condition may stimulate NADPH oxidases. This crosstalk between mitochondria and NADPH oxidases, therefore, may represent a feed-forward vicious cycle of ROS production which can be pharmacologically targeted under conditions of oxidative stress. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions.

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Induced expression of manganese superoxide dismutase by non-toxic concentrations of oxidized low-density lipoprotein (oxLDL) protects against oxLDL-mediated cytotoxicity

Cited by 31 publications

References 47 publications

Chromium and Manganese Levels in Biological Samples of Pakistani Myocardial Infarction Patients at Different Stages as Related to Controls

Chromium and Manganese Levels in Biological Samples of Pakistani Myocardial Infarction Patients at Different Stages as Related to Controls

Oxidized LDL induces mitochondrially associated reactive oxygen/nitrogen species formation in endothelial cells

Cross talk between mitochondria and NADPH oxidases

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