Malondialdehyde, a Lipoperoxidation-Derived Aldehyde, Can Bring About Secondary Oxidative Damage To Proteins

Traverso, Nicola; Menini, Stefano; Maineri, Elena Pesce; Patriarca, Stefania; Odetti, Patrizio; Cottalasso, Damiano; Marinari, Umberto M.; Pronzato, Maria Adelaide

doi:10.1093/gerona/59.9.b890

Cited by 116 publications

(61 citation statements)

References 47 publications

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“…These findings indicated that excessive oxidative stress occurred during the AngII stimulation process. However, probucol treatment significantly reduced the MDA concentration and increased total SOD activity, suggesting that probucol had potent antioxidative properties, which is supported by a previous study (23). The protective effect of probucol against atherosclerosis may partly be due to its ability to lower MDA concentrations or increase antioxidant enzyme activities (24).…”

Section: Discussionsupporting

confidence: 71%

Effects of probucol on angiotensin II-induced BMP-2 expression in human umbilical vein endothelial cells

Zhang

Wang

Liu

et al. 2012

Molecular Medicine Reports

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Abstract. Bone morphogenetic protein-2 (BMP-2) participates significantly in vascular development and pathophysiological processes. Angiotensin II (AngII) has been demonstrated to be critical in the initiation and progression of atherosclerosis. However, the effects of AngII on BMP-2 expression and of probucol on the AngII-induced BMP-2 expression in human umbilical vein endothelial cells (HUVECs) are unknown. The aim of our study was to investigate these effects. HUVECs were cultured and stimulated with various agents. The total superoxide dismutase (SOD) activity and the concentrations of malondialdehyde (MDA) and BMP-2 were measured by standard methods. Northern blotting was used to detect the expression of BMP-2 mRNA. The activation of NF-κB in the HUVECs was also determined. The AngII treatment significantly increased BMP-2 expression levels and activated NF-κB. These effects were suppressed by treatment with pyrrolidine dithiocarbamate (PDTC) or probucol. Furthermore, the increased levels of MDA in the conditioned medium and the decrease in the total SOD activity caused by the AngⅡ treatment were reversed by treatment with probucol or PDTC. Probucol downregulated the AngII-induced BMP-2 expression. These effects of probucol may be mediated by the inhibition of NF-κB activation.

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Section: Discussionsupporting

confidence: 71%

Effects of probucol on angiotensin II-induced BMP-2 expression in human umbilical vein endothelial cells

Zhang

Wang

Liu

et al. 2012

Molecular Medicine Reports

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“…One of best histochemically detectable markers of oxidative stress in tissues is MDA, which appears during lipid peroxidation of cell membranes (53,59). After it is produced, MDA forms adducts with specific proteins in cells.…”

Section: On April 1 2019 By Guestmentioning

confidence: 99%

Retrovirus-Induced Oxidative Stress with Neuroimmunodegeneration Is Suppressed by Antioxidant Treatment with a Refined Monosodium α-Luminol (Galavit)

Jiang

Scofield

Yan

et al. 2006

J Virol

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Oxidative stress is involved in many human neuroimmunodegenerative diseases, including human immunodeficiency virus disease/AIDS. The retrovirus ts1, a mutant of Moloney murine leukemia virus, causes oxidative stress and progressive neuro-and immunopathology in mice infected soon after birth. These pathological changes include spongiform neurodegeneration, astrogliosis, thymic atrophy, and T-cell depletion. Astrocytes and thymocytes are directly infected and killed by ts1. Neurons are not infected, but they also die, most likely as an indirect result of local glial infection. Cytopathic effects of ts1 infection in cultured astrocytes are associated with accumulation of the viral envelope precursor protein gPr80 env in the endoplasmic reticulum (ER), which triggers ER stress and oxidative stress. We have reported (i) that activation of the Nrf2 transcription factor and upregulation of antioxidative defenses occurs in astrocytes infected with ts1 in vitro and (ii) that some ts1-infected astrocytes survive infection by mobilization of these pathways. Here, we show that treatment with a refined monosodium ␣-luminol (Galavit; GVT) suppresses oxidative stress and Nrf2 activation in cultured ts1-infected astrocytes. GVT treatment also inhibits the development of spongiform encephalopathy and gliosis in the central nervous system (CNS) in ts1-infected mice, preserves normal cytoarchitecture in the thymus, and delays paralysis, thymic atrophy, wasting, and death. GVT treatment of infected mice reduces ts1-induced oxidative stress, cell death, and pathogenesis in both the CNS and thymus of treated animals. These studies suggest that oxidative stress mediates ts1-induced neurodegeneration and T-cell loss.

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“…However, PDTC or irbesartan treatment significantly reduced MDA concentration, suggesting that irbesartan had a strong antioxidative property, which was supported by the previous study. 29 In conclusion, Ang II-induced BMP-2 expression was suppressed by PDTC or irbesartan treatment. Ang II-induced BMP-2 expression might involve excessive oxidative stress.…”

Section: Induction Of Bmp-2 and Cuznsod Expression In Huvecsmentioning

confidence: 80%

Irbesartan attenuates Ang II-induced BMP-2 expression in human umbilical vein endothelial cells

et al. 2008

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Bone morphogenetic protein-2 (BMP-2), a transforming growth factor-β superfamily member cytokine, plays a key role both in vascular development and in pathophysiological processes. However, the effects and mechanisms of angiotensin II (Ang II) on BMP-2 expression remain unknown in human umbilical vein endothelial cells (HUVECs). Here we show that Ang II treatment significantly increased BMP-2 expression, associated with NF-κB activation, which was suppressed by treatment with pyrrolidine dithiocarbamate (PDTC) or irbesartan. Furthermore, the increased levels of MDA (malondialdehyde) in conditioned media and the decrease in activities of total superoxide dismutases (SOD) caused by Ang II were reversed by irbesartan or PDTC treatment. Our findings indicate that Ang II-induced BMP-2 expression might contribute to NF-κB activation. BMP-2 expression induced by Ang II might involve excessive oxidative stress.

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Malondialdehyde, a Lipoperoxidation-Derived Aldehyde, Can Bring About Secondary Oxidative Damage To Proteins

Cited by 116 publications

References 47 publications

Effects of probucol on angiotensin II-induced BMP-2 expression in human umbilical vein endothelial cells

Effects of probucol on angiotensin II-induced BMP-2 expression in human umbilical vein endothelial cells

Retrovirus-Induced Oxidative Stress with Neuroimmunodegeneration Is Suppressed by Antioxidant Treatment with a Refined Monosodium α-Luminol (Galavit)

Irbesartan attenuates Ang II-induced BMP-2 expression in human umbilical vein endothelial cells

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