Overexpression of the transgene for manganese superoxide dismutase (MnSOD) in 32D cl 3 cells prevents apoptosis induction by TNF-α, IL-3 withdrawal, and ionizing radiation

Epperly, Michael W.; Bernarding, Michael; Gretton, Joan; Jefferson, Mia; Nie, Suhua; Greenberger, Joel S.

doi:10.1016/s0301-472x(03)00041-9

Cited by 57 publications

(31 citation statements)

References 45 publications

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“…It has been reported that mitochondria are major contributors to ROS formation [22]. It is noteworthy to note that SOD2 is a crucial The mRNAs for SOD2, SOD1, and NQO1 measured by real-time quantitative RT-PCR were normalized by the internal standard, RPL13A mRNA, and expressed relative to the value in the control group a Each value is the mean ± SD of three independent experiments from triplicate samples ** P \ 0.01, versus the control group mitochondrial antioxidant enzyme, which binds to the superoxide byproducts of oxidative phosphorylation and converts them to hydrogen peroxide and diatomic oxygen, thus protecting the cells against oxidative stress [24][25][26]. Taken together, this evidence suggests that mitochondrial pathways play a crucial role in the effects of arsenic on HUVECs, and in the development of peripheral vascular diseases.…”

Section: Discussionmentioning

confidence: 99%

“…SOD2 is a mitochondrial enzyme, which binds to the superoxide byproducts of oxidative phosphorylation and converts them to hydrogen peroxide and diatomic oxygen. SOD3 is an extracellular enzyme that is secreted into the extracellular space and anchored to the extracellular matrix (ECM) and cell surfaces through an interaction with heparan sulfate proteoglycan and collagen, thus protecting tissues from oxidative stress [24][25][26]. NAD(P)H:quinone oxidoreductase 1 (NQO1) is a FAD-binding cytoplasmic reductase that forms homodimer and catalyzes the detoxification of quinones and their derivatives, thus preventing their participation in redox cycling and oxidative stress [27,28].…”

Section: Introductionmentioning

confidence: 99%

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Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

Shi

Wei

et al. 2010

Cardiovasc Toxicol

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To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels, we analyzed the effects of sodium arsenite (NaAsO(2)) on the apoptosis of human umbilical vein endothelial cells (HUVECs), mitochondrial membrane potential (Delta Psi m), intracellular reactive oxygen species (ROS), and the expression of the related genes. HUVECs apoptosis increased and Delta Psi m decreased in a dose-dependent manner following arsenic treatment. Intracellular ROS showed 2 phase alterations: a slight decrease with low levels of arsenic (5 and 10 microM) treatment; but a sharp increase at higher concentrations (>or=20 microM). The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-L-cysteine (NAC). The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment. Based on the results, we suggest that the decrease of Delta Psi m caused by arsenic and the resulting cell apoptosis may contribute to the injuries of blood vessel in arsenism. The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO(2), suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

Shi

Wei

et al. 2010

Cardiovasc Toxicol

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“…In consistent with its cellular function, the MnSOD knockout mice die embryonically and are hypersensitive to apoptosis (4,5). Furthermore, the over-expression of MnSOD blocks apoptosis induced by praline oxidase, TNF-α, IL-3 withdrawal or ionizing irradiation (6)(7)(8)(9). During Fas-mediated apoptosis, MnSOD is inactivated by caspase-specific degradation (10).…”

Section: Introductionmentioning

confidence: 93%

The subcellular distribution of MnSOD alters during sodium selenite-induced apoptosis

Guan¹,

Jiang²,

Li³

et al. 2009

BMB Reports

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“…2). Manganese is an essential element for all types of tissue, and plays important roles in the free radical defense system as manganese superoxide dismutase (MnSOD), which protects mitochondria from damage by superoxide radicals [8, 9]. Eosinophils have been reported to undergo apoptosis by reactive oxygen species (ROS) [10], and MnSOD is involved in the inhibition of eosinophil apoptosis [11].…”

Section: Resultsmentioning

confidence: 99%

Effects of Nickel on Eosinophil Survival

Ishihara

Goi²,

Hong³

et al. 2009

Int Arch Allergy Immunol

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Background: Accessories, watches, coins and other items containing metal sometimes cause contact dermatitis and metal allergy. Among metals, nickel in alloys is ionized by sweat on the surface of the skin and exhibits particularly marked irritancy and allergenicity. Although eosinophils play important roles in allergy, the effects of nickel on eosinophils have not been elucidated. Methods: Eosinophils were prepared from the peritoneal cavity in rats immunized with Ascaris suum extract. Purified rat eosinophils were incubated in the presence of various kinds of metals including nickel. The viability of eosinophils was analyzed using a flow cytometer. Results: When rat eosinophils were incubated for 3 days in the presence of nickel chloride at 30–1,000 μM, the viability of eosinophils was decreased in a concentration-dependent manner. Nickel chloride at 300 μM significantly increased the percentage of annexin V⁺ PI^– eosinophils. The population of annexin V⁺ PI^– eosinophils was also increased by nickel sulfate, cobalt chloride and zinc sulfate. The binding of nickel ions to eosinophils was detected by flow cytometer. Conclusions: Nickel ions bind to eosinophils and decrease the viability of eosinophils through the induction of apoptosis. Nickel ions may exhibit activity which modifies the function of eosinophils in allergy.

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Overexpression of the transgene for manganese superoxide dismutase (MnSOD) in 32D cl 3 cells prevents apoptosis induction by TNF-α, IL-3 withdrawal, and ionizing radiation

Cited by 57 publications

References 45 publications

Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

The subcellular distribution of MnSOD alters during sodium selenite-induced apoptosis

Effects of Nickel on Eosinophil Survival

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