Satratoxin H Generates Reactive Oxygen Species and Lipid Peroxides in PC12 Cells

Nusuetrong, Punnee; Pengsuparp, Thitima; Meksuriyen, Duangdeun; Tanitsu, Masa‐aki; Kikuchi, Haruhisa; Mizugaki, Michinao; Shimazu, Ken Ichi; Oshima, Yoshiteru; Nakahata, Norimichi; Yoshida, Makoto

doi:10.1248/bpb.31.1115

Cited by 14 publications

(15 citation statements)

References 53 publications

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“…Numerous researchers have shown that ROS relate to apoptosis that is processed through the mitochondrial pathway, which depends on the activation of p38 (Figure 2) [40][41][42][43][44] . Apoptosis signal-regulating kinase 1 (ASK1) is an evolutionarily conserved mitogenactivated protein 3-kinase that activates both JNK and p38 MAPK, which may also be triggered by ROS [45][46][47][48][49] .…”

Section: Ros Involve Apoptosis That Relates To the P38 Pathwaymentioning

confidence: 99%

Reactive oxygen species: A double-edged sword in oncogenesis

Pan¹,

Hong²,

Ren³

2009

WJG

206

133

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Reactive oxygen species (ROS) are molecules or ions formed by the incomplete one-electron reduction of oxygen. Of interest, it seems that ROS manifest dual roles, cancer promoting or cancer suppressing, in tumorigenesis. ROS participate simultaneously in two signaling pathways that have inverse functions in tumorigenesis, Ras-Raf-MEK1/2-ERK1/2 signaling and the p38 mitogen-activated protein kinases (MAPK) pathway. It is well known that Ras-Raf-MEK1/2-ERK1/2 signaling is related to oncogenesis, while the p38 MAPK pathway contributes to cancer suppression, which involves oncogene-induced senescence, inflammationinduced cellular senescence, replicative senescence, contact inhibition and DNA-damage responses. Thus, ROS may not be an absolute carcinogenic factor or cancer suppressor. The purpose of the present review is to discuss the dual roles of ROS in the pathogenesis of cancer, and the signaling pathway mediating their role in tumorigenesis.

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Section: Ros Involve Apoptosis That Relates To the P38 Pathwaymentioning

confidence: 99%

Reactive oxygen species: A double-edged sword in oncogenesis

Pan¹,

Hong²,

Ren³

2009

WJG

206

133

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“…Previously, we demonstrated that satratoxin H caused the apoptosis in PC12 cells with the IC 50 of approximately 50 nM through MAPK (Nusuetrong et al, 2005) and ROS generation (Nusuetrong et al, 2008). We further showed that satratoxin H induced DNA fragmentation in PC12 cells (Nusuetrong et al, 2008).…”

Section: Introductionmentioning

confidence: 78%

“…We further showed that satratoxin H induced DNA fragmentation in PC12 cells (Nusuetrong et al, 2008). However, although DNA is triggered single-stranded or double-stranded breaks, a mechanism of satratoxin H on DNA damage is unknown.…”

Section: Introductionmentioning

confidence: 80%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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-Satratoxin H is an important air-and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that satratoxin H induced chromosome break. Also, satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of satratoxin H.

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“…Satratoxin H is thought to induce apoptosis of PC12 cells through the activation of p38 mitogen activated protein kinase and c-Jun N-terminal kinase in GSH-sensitive manner [173]. Chemoprotective effects of flavonoid compounds against aflatoxins were confirmed in hens [174].…”

Section: Mmycotoxins and Apoptosismentioning

confidence: 97%

Mycotoxins-Induced Oxidative Stress and Disease

Omar¹

2013

Mycotoxin and Food Safety in Developing Countries

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Satratoxin H Generates Reactive Oxygen Species and Lipid Peroxides in PC12 Cells

Cited by 14 publications

References 53 publications

Reactive oxygen species: A double-edged sword in oncogenesis

Reactive oxygen species: A double-edged sword in oncogenesis

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Mycotoxins-Induced Oxidative Stress and Disease

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