Broccoli: A Unique Vegetable That Protects Mammalian Hearts through the Redox Cycling of the Thioredoxin Superfamily

Mukherjee, Subhendu; Gangopadhyay, Hiranmoy; Das, Dipak K.

doi:10.1021/jf0728146

Cited by 109 publications

(94 citation statements)

References 46 publications

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“…broccoli-enriched diet exhibit significant increases in aortic smooth muscle mitochondrial proteins that could influence PTP opening, including thioredoxin, thioredoxin reductase, glutathione reductase, glutathione, and catalase enzyme activities (Mukherjee et al, 2008). Mitochondria isolated from the livers of rats injected intraperitoneally 40 hours earlier with sulforaphane exhibit elevated immunoreactive levels of glutathione peroxidase 1, thioredoxin 2, and mitochondrial malic enzyme (Greco et al, 2011).…”

Section: Protection Against Mitochondrial Oxidative Stressmentioning

confidence: 99%

Novel Mitochondrial Targets for Neuroprotection

Pérez-Pinzón

Stetler

Fiskum

2012

J Cereb Blood Flow Metab

130

108

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Mitochondrial dysfunction contributes to the pathophysiology of acute neurologic disorders and neurodegenerative diseases. Bioenergetic failure is the primary cause of acute neuronal necrosis, and involves excitotoxicity-associated mitochondrial Ca 2 + overload, resulting in opening of the inner membrane permeability transition pore and inhibition of oxidative phosphorylation. Mitochondrial energy metabolism is also very sensitive to inhibition by reactive O 2 and nitrogen species, which modify many mitochondrial proteins, lipids, and DNA/RNA, thus impairing energy transduction and exacerbating free radical production. Oxidative stress and Ca 2 + -activated calpain protease activities also promote apoptosis and other forms of programmed cell death, primarily through modification of proteins and lipids present at the outer membrane, causing release of proapoptotic mitochondrial proteins, which initiate caspase-dependent and caspase-independent forms of cell death. This review focuses on three classifications of mitochondrial targets for neuroprotection. The first is mitochondrial quality control, maintained by the dynamic processes of mitochondrial fission and fusion and autophagy of abnormal mitochondria. The second includes targets amenable to ischemic preconditioning, e.g., electron transport chain components, ion channels, uncoupling proteins, and mitochondrial biogenesis. The third includes mitochondrial proteins and other molecules that defend against oxidative stress. Each class of targets exhibits excellent potential for translation to clinical neuroprotection.

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Section: Protection Against Mitochondrial Oxidative Stressmentioning

confidence: 99%

Novel Mitochondrial Targets for Neuroprotection

Pérez-Pinzón

Stetler

Fiskum

2012

J Cereb Blood Flow Metab

130

108

View full text Add to dashboard Cite

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“…Nrf2 is widely expressed and it has been studied in many different tissues [7,33,34] . In the cardiovascular system, it has been shown that ischemia/ reperfusion (I/R) down-regulates Nrf2 protein expression in rat heart and that aging decreases glutathione synthesis via diminished Nrf2 signaling in rat vascular endothelial and smooth muscle cells, suggesting that Nrf2 may play a critical role in the development of CVD in the aged population [6,35] . He et al [30] have shown a functionally decreased contractility when Nrf2 is genetically deleted from cardiomyocytes due to a marked increase in high-glucose oxidative stress and apoptosis.…”

Section: Signalingmentioning

confidence: 99%

“…Several animal models suggest that when endogenous anti-oxidant systems are overwhelmed, exogenous antioxidant supplementation can be used for preventive and/or therapeutic intervention of oxidative cardiovascular disorders [35,36] . Phenolic acids are a group of compounds that are widely distributed in natural plant foods including fruits, vegetables and whole grains [36] .…”

Section: Role Of Nutrition In Antioxidant Signalingmentioning

confidence: 99%

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Effects of interventions on oxidative stress and inflammation of cardiovascular diseases

Lee¹,

Park²,

Zuidema³

et al. 2011

WJC

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Excessive oxidative stress and low-grade chronic inflammation are major pathophysiological factors contributing to the development of cardiovascular diseases (CVD) such as hypertension, diabetes and atherosclerosis. Accumulating evidence suggests that a compromised antioxidant system can lead to excessive oxidative stress in cardiovascular related organs, resulting in cell damage and death. In addition, increased circulating levels of pro-inflammatory cytokines, such as tumor necrosis factor α, interleukin-6 and C-reactive protein, are closely related to morbidity and mortality of cardiovascular complications. Emerging evidence suggests that interventions including nutrition, pharmacology and exercise may activate expression of cellular anti-oxidant systems via the nuclear factor erythroid 2-related factor 2-Kelchlike ECH-associated protein 1 signaling pathway and play a role in preventing inflammatory processes in CVD. The focus of the present review is to summarize recent evidence showing the role of these anti-oxidant and anti-inflammatory interventions in cardiovascular disease. We believe that these findings may prompt new effective pathogenesis-oriented interventions, based on the exercise-induced protection from disease in the cardiovascular system, aimed at targeting oxidant stress and inflammation.

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“…Possible explanations for this indirect effect of sulforaphane include increased expression of mitochondrial enzymes that reduce NADP + to NADPH [105] and increased expression of the anti-apoptotic mitochondrial protein, Bcl-2. Cardiac Bcl-2 levels are elevated in rats maintained on a high broccoli diet [106]. Moreover, we have shown that mitochondria within Bcl-2 overexpressing neural cell lines are resistant to PTP opening [107].…”

Section: S433mentioning

confidence: 81%

Neuroprotection through Stimulation of Mitochondrial Antioxidant Protein Expression

Greco

Fiskum

2010

JAD

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Abstract. Oxidative stress and loss of cellular Ca2+ homeostasis are closely linked and are common denominators in the pathophysiology of many neurodegenerative diseases and acute disorders of the nervous system. Mitochondria are major targets of oxidative stress and abnormal intracellular Ca 2+ , as both can cause bioenergetic failure through synergistic activation of the mitochondrial inner membrane permeability transition pore. Opening of this molecularly ill-defined pore causes both collapse of the membrane potential, which drives oxidative phosphorylation, and release of small metabolites, including pyridine nucleotides and glutathione, which are necessary for energy metabolism and defense against oxidative stress. Expression of genes coding for many antioxidant defense proteins is regulated by the Nrf2 transcriptional activating factor. Translocation of this protein from the cytosol to the nucleus is stimulated by oxidative stress and by specific agents that either react with cysteine sulfhydryl groups present on the protein KEAP1, that normally binds and restricts Nrf2 translocation, or that stimulate serine phosphorylation of Nrf2. Recent evidence indicates that mitochondria are a target of the cytoprotective gene expression induced by Nrf2 and that this pathway can increase resistance to redox-regulated opening of the permeability transition pore. Pharmacologic stimulation of the Nrf2 system and its protection against mitochondrial bioenergetic dysfunction may therefore constitute a powerful mechanism for both pre-conditioning against neurodegeneration and for post-conditioning against neural cell death associated with acute neurologic injury.Keywords: Antioxidant, bioenergetics, calcium, cerebral ischemia, neurodegeneration, Nrf2, oxidative stress, permeability transition pore are located at mitochondria or that are extramitochondrial but have strong secondary effects on mitochondrial bioenergetic or apoptotic activities. The most acute influence of ROS/RNS on mitochondria is mediated by oxidative modifications of proteins present in the electron transport chain (ETC) [1,2], other metabolic proteins, e.g., pyruvate dehydrogenase aconitase and α-ketogluatarate dehydrogenase [3][4][5], and the inner membrane permeability transition pore (PTP) [6,7]. Oxidation of cardiolipin, a phospholipid primarily lo- OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN NEURODEGENERATION

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Broccoli: A Unique Vegetable That Protects Mammalian Hearts through the Redox Cycling of the Thioredoxin Superfamily

Cited by 109 publications

References 46 publications

Novel Mitochondrial Targets for Neuroprotection

Novel Mitochondrial Targets for Neuroprotection

Effects of interventions on oxidative stress and inflammation of cardiovascular diseases

Neuroprotection through Stimulation of Mitochondrial Antioxidant Protein Expression

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