Menadione-induced cytotoxicity to rat osteoblasts

Sun, Jui‐Sheng; Tsuang, Yang Hwei; Huang, Wan-Ching; Chen, L T; Hang, Yi‐Shiong; Lu, Fung‐Jou

doi:10.1007/s000180050118

Cited by 32 publications

(18 citation statements)

References 52 publications

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“…Results from our study suggest that physical ESW promotes bone marrow stromal cell growth and differentiation toward osteoprogenitor as a result of early O 2 Ϫ -mediated TGF-␤1 induction. In contrast to previous studies showing that a large quantity of O 2 Ϫ or ONOO Ϫ from skeletal injury or cytotoxic agent was cytotoxic to osteoblasts (55,56), we have showed that ESWpromoted osteoprogenitor cell growth was mediated by O 2 Ϫ production. Superoxide can easily react with NO to generate ONOO Ϫ for the regulation of cell growth at less toxic levels (57).…”

Section: Discussioncontrasting

confidence: 99%

Superoxide Mediates Shock Wave Induction of ERK-dependent Osteogenic Transcription Factor (CBFA1) and Mesenchymal Cell Differentiation toward Osteoprogenitors

Wang

Sheen-Chen

et al. 2002

Journal of Biological Chemistry

159

126

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؊ by superoxide dismutase and inhibition of ERK activation by PD98059 decreased specific osteogenic transcription factor, core binding factor A1 activation, and decreased osteocalcin expression. Taken together, we showed that ESW-induced O 2 ؊ production followed by tyrosine kinase-mediated ERK activation and core binding factor A1 activation resulted in osteogenic cell growth and maturation. Thus, an appropriate modulation of redox reaction by ESW may have some positive effect on the bone regeneration.Oxidative stress induced by superoxide has been implicated in the induction of certain cell injury (1-5). In contrast, superoxide also plays an important role in the regulation of cell proliferation and metabolism (6 -8). Several physical factors such as heat (9), electrical field (10), pulsatile stretch (11), and laser irradiation (12) can stimulate cell proliferation through the involvement of superoxide. It is not known whether superoxide can regulate osteoprogenitor cell growth and differentiation.Extracorporeal shock wave (ESW) 1 is created by a high voltage spark discharge under water causing an explosive evaporation of water and producing high energy acoustic waves. The acoustic waves are focused on a semi-ellipsoid reflector and therefore can be transmitted into a specific tissue site (13). ESW treatment has been divergently applied for eukaryotic and prokaryotic biology systems. It is well known that ESW provides a non-invasive biophysical strategy for breaking renal stones with minimal side effects (13). Evidence also suggests that shock waves can potentially enhance gene transfer (14), suppress tumor growth (15), and promote the bactericidal effect of microorganisms (16).Recently, we and others (17)(18)(19)(20) have shown that ESW treatment has a promising effect on the promotion of bone fracture healing and repair of tendinitis. The mechanism by which ESW enhances fracture healing and repair of tendinitis remains to be determined. The fact that ESW treatment enhances both bone and tendon regeneration suggests that ESW may induce a certain signal for growth and maturation of the mesenchymal progenitors from bone marrow. It has been well clarified that the differentiation and maturation of bone marrow mesenchymal osteoprogenitor cells into osteoblastic lineage is involved in bone regeneration (21)(22)(23). In support of the hypothesis, we have recently shown ESW treatment to be able to promote bone marrow stromal cell growth and differentiation toward osteogenic lineage, presumably through TGF-␤1 induction (24).Accumulated evidence suggests that ESW induces a cavitation effect to increase membrane permeability and the influx of biological substances (25,26), which are usually implicated in cell and tissue damage (15,27). There is limited evidence showing that ESW promotes cell growth rather than cell damage. We hypothesized in this study that an optimal ESW treatment promoted osteoprogenitor cell growth and maturation via a rapid induction of oxygen radicals for a signal transduction

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Section: Discussioncontrasting

confidence: 99%

Superoxide Mediates Shock Wave Induction of ERK-dependent Osteogenic Transcription Factor (CBFA1) and Mesenchymal Cell Differentiation toward Osteoprogenitors

Wang

Sheen-Chen

et al. 2002

Journal of Biological Chemistry

159

126

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“…Along with cell growth inhibition, previous work shows that VK 3 -induced cell death is by apoptosis (30,33), at least within certain doses; excessive doses induce necrosis rather than apoptosis (23,34). We have confirmed this result in the Jurkat subclone E6-1, derived from a human acute T cell leukemia.…”

Section: Discussionsupporting

confidence: 87%

Apoptosis Provoked by the Oxidative Stress Inducer Menadione (Vitamin K3) Is Mediated by the Fas/Fas Ligand System

Caricchio

Kovalenko

Kaufmann

et al. 1999

Clinical Immunology

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“…Menadione (100 M) was added after the medium was autoclaved. (Note that the concentration of menadione used in oxidative stress studies is usually 50 to 500 M [35,38,40].) The media were then inoculated with 1 ml of stationary-phase cells grown in a medium not amended with menadione on an aerated gyratory water bath shaker (model 76; New Brunswick Scientific) at 26°C at 140 rpm.…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress Evokes a Metabolic Adaptation That Favors Increased NADPH Synthesis and Decreased NADH Production in Pseudomonas fluorescens

et al. 2007

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The fate of all aerobic organisms is dependent on the varying intracellular concentrations of NADH and NADPH. The former is the primary ingredient that fuels ATP production via oxidative phosphorylation, while the latter helps maintain the reductive environment necessary for this process and other cellular activities. In this study we demonstrate a metabolic network promoting NADPH production and limiting NADH synthesis as a consequence of an oxidative insult. The activity and expression of glucose-6-phosphate dehydrogenase, malic enzyme, and NADP ؉ -isocitrate dehydrogenase, the main generators of NADPH, were markedly increased during oxidative challenge. On the other hand, numerous tricarboxylic acid cycle enzymes that supply the bulk of intracellular NADH were significantly downregulated. These metabolic pathways were further modulated by NAD ؉ kinase (NADK) and NADP ؉ phosphatase (NADPase), enzymes known to regulate the levels of NAD ؉ and NADP ؉ . While in menadione-challenged cells, the former enzyme was upregulated, the phosphatase activity was markedly increased in control cells. Thus, NADK and NADPase play a pivotal role in controlling the cross talk between metabolic networks that produce NADH and NADPH and are integral components of the mechanism involved in fending off oxidative stress.If an aerobic organism is to survive, it is essential that an adequate supply of NADPH is available. This nicotinamide nucleotide provides a reductive environment that enables the oxidative cell to nullify the reactive oxygen species (ROS) generated as a consequence of oxidative phosphorylation, a process key to the generation of ATP (9,18,22). All organisms that utilize oxygen as the terminal e Ϫ acceptor have evolved intricate molecular strategies that allow them to combat the inherent dangers associated with living in an aerobic environment (11,26). Catalase, superoxide dismutase (SOD), and glutathione peroxidase are some of the enzymes that help decrease oxidative tension during aerobic respiration (4). However, the effectiveness of these proteins as the scavengers of ROS depends on the availability of NADPH. This nucleotide supplies the reductive power necessary to quell the oxidative potential of ROS. Hence, the production of this reducing agent is an integral part of the oxidative energy-generating machinery of all aerobic organisms. Production of ATP via oxidative phosphorylation cannot proceed effectively in the absence of a continual supply of NADPH (14, 31).Glucose-6-phosphate dehydrogenase (G6PDH), NADP ϩ -isocitrate dehydrogenase (ICDH-NADP ϩ ), malic enzyme (ME), 6-phosphogluconate dehydrogenase (6PGDH), and glutamate dehydrogenase-NADP ϩ (GDH-NADP ϩ ) are some of the important enzymes that enable aerobic cells to fulfill their requirement for NADPH (34). NADH, which is generated essentially during the catabolism of acetyl-coenzyme A via the tricarboxylic acid (TCA) cycle, is a potent prooxidant as its downstream metabolism mediated by complexes I, III, and IV produces the majority of the ROS generated in...

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Menadione-induced cytotoxicity to rat osteoblasts

Cited by 32 publications

References 52 publications

Superoxide Mediates Shock Wave Induction of ERK-dependent Osteogenic Transcription Factor (CBFA1) and Mesenchymal Cell Differentiation toward Osteoprogenitors

Superoxide Mediates Shock Wave Induction of ERK-dependent Osteogenic Transcription Factor (CBFA1) and Mesenchymal Cell Differentiation toward Osteoprogenitors

Apoptosis Provoked by the Oxidative Stress Inducer Menadione (Vitamin K3) Is Mediated by the Fas/Fas Ligand System

Oxidative Stress Evokes a Metabolic Adaptation That Favors Increased NADPH Synthesis and Decreased NADH Production in Pseudomonas fluorescens

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