Dominant roles of Fenton reaction in sodium nitroprusside-induced chondrocyte apoptosis

Quan, Yingyao; Qin, Guiqi; Huang, Hao; Liu, Yuhong; Wang, Xiaoping; Chen, Tongsheng

doi:10.1016/j.freeradbiomed.2016.02.026

Cited by 25 publications

(33 citation statements)

References 57 publications

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“…In contrast, PTIO pretreatment did not prevent SNP-induced cytotoxicity in Hep3B cells (Figure 2A), demonstrating that NO was not participate in SNP-induced cytotoxicity of Hep3B cells. Our previous study has indicated that 24-h-photodegreaded SNP (SNPex) released NO moiety completely [23]. We here found that SNP induced much more cytotoxicity (Figure 2B) than SNPex in HepG2 cells, further confirming the key role of NO in SNP-induced apoptosis in this cell line.…”

Section: Resultssupporting

confidence: 81%

“…Further experiments in Hep3B cells show that ROS instead of NO play a dominant role in SNP-induced apoptosis in this cell line (private data), which is similar to our recent report in chondrocytes [23]. Therefore, we here focus on exploring how SNP induces apoptosis in HepG2 cells.…”

Section: Resultssupporting

confidence: 76%

“…However, many studies have demonstrated that the direct toxicity of NO is very modest [27, 33]. Our recent study also showed that although SNP induced NO generation, ROS instead of NO mediated SNP-induced chondrocytes apoptosis [23]. Moreover, NOC-5 which induced more 50-fold than the SNP-induced NO production exhibited much lower cytotoxicity than that of SNP in chondrocytes [23].…”

Section: Discussionmentioning

confidence: 97%

“…This notion was widely adopted to study the molecular mechanism of SNP-induced apoptosis in various cell lines [20–22]. However, we and other research groups found that reactive oxygen species (ROS), the by-product of SNP independent of NO, mediated SNP-induced cytotoxicity in various kinds of cells [23–29]. Our recent studies firmly demonstrated that hydroxyl radicals ( · OH) from the Fenton reaction between iron ions and hydrogen peroxide (H 2 O 2 ) dominated the SNP-induced NO-independent chondrocytes apoptosis though SNP induced NO production [23].…”

Section: Introductionmentioning

confidence: 99%

“…However, we and other research groups found that reactive oxygen species (ROS), the by-product of SNP independent of NO, mediated SNP-induced cytotoxicity in various kinds of cells [23–29]. Our recent studies firmly demonstrated that hydroxyl radicals ( · OH) from the Fenton reaction between iron ions and hydrogen peroxide (H 2 O 2 ) dominated the SNP-induced NO-independent chondrocytes apoptosis though SNP induced NO production [23]. Based on the potent inhibitory effect of uric acid, an ONOO − scavenger, on the cytotoxicity of SNP in mouse macrophage-like RAW264.7 cells some researchers speculated that ONOO − might play a key role in SNP-induced cytotoxicity [30, 31].…”

Section: Introductionmentioning

confidence: 99%

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Peroxynitrite dominates sodium nitroprusside-induced apoptosis in human hepatocellular carcinoma cells

et al. 2017

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This study aims to explore which radicals dominate sodium nitroprusside (SNP)-induced cytotoxicity in human hepatocellular carcinoma (HCC) cells (HepG2 and Hep3B). Exposure of SNP to cell medium produced abundant nitric oxide (NO), superoxide anion (O2·−), hydrogen peroxide (H2O2) and iron ions. SNP potently induced caspases activation, mitochondrial membrane permeabilization and apoptosis in HCC cells. In Hep3B cells, pretreatment with NO scavenger (PTIO) did not prevent SNP-induced cytotoxicity. However, in HepG2 cells, SNP-induced cytotoxicity was prevented significantly by pretreatment with PTIO and O2·− scavenger, and especially was almost completely blocked by pretreatment with FeTPPS (peroxynitrite scavenger). In contrast, although H2O2 scavenger potently scavenged SNP-induced H2O2 production, it did not prevent SNP-induced cytotoxicity in HepG2 cells. In addition, pretreatment with DFO (iron ions chelator) and iron-saturated DFO respectively completely prevented SNP-induced cytotoxicity in HepG2 cells. Collectively, peroxynitrite from the reaction between NO and O2·− elicited from SNP dominates the SNP-induced apoptosis of HepG2 cells, in which both iron ions and H2O2 are not involved.

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Section: Resultssupporting

confidence: 81%

Section: Resultssupporting

confidence: 76%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Peroxynitrite dominates sodium nitroprusside-induced apoptosis in human hepatocellular carcinoma cells

et al. 2017

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Role of ATP5G3 in sodium nitroprusside‐induced cell death in cervical carcinoma cells

Lee

Rim

Lee

et al. 2022

J Biochem & Molecular Tox

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We identified a gene, subunit C3 (ATP5G3) of mitochondrial ATP synthase, that displayed changes in gene expression under oxidative stress. We examined the role of ATP5G3 and its molecular mechanisms in sodium nitroprusside (SNP)-induced cell death using ATP5G3 small interfering RNA (siATP5G3)-transfected HeLa cells. A significant increase in cytotoxicity was observed in the transfected cells treated with SNP, which suggests a protective role of ATP5G3 in SNP-induced cytotoxicity in the cells. The transfected cells treated with photodegraded SNP showed equal cytotoxicity to SNP, and pretreatment with deferoxamine (DFO) completely inhibited this cytotoxicity. Further, cytotoxicity was significantly inhibited by pretreatment with a p38 inhibitor and was accentuated by the p38 activator in cells. Pretreatment with the Bcl-xL inhibitor also significantly accentuated cytotoxicity. The increase in p38 phosphorylation was significantly higher in siATP5G3-transfected cells treated with SNP in immunoblotting, which was inhibited by pretreatment with DFO. The increase in cytotoxicity with siATP5G3 transfection was completely blocked by cotransfection with sip38, and the blocking effect disappeared by cotransfection with additional siBcl-xL, which suggests that the protective role of ATP5G3 is mediated by Bcl-xL via the inhibition of p38 activity. Cytotoxicity was completely blocked by the cotransfection of siATP5G3 with siBax. No change in apoptotic parameters was observed during cytotoxicity.However, pretreatment with lysosomal inhibitors significantly inhibited cytotoxicity and increased p62 protein levels. These findings suggest that ATP5G3 plays a protective role in autophagic cell death/lysosome-associated cell death induced by SNP via the sequential signaling of ROS/p38/Bcl-xL/Bax in HeLa cells.

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Intracellular catalase activity instead of glutathione level dominates the resistance of cells to reactive oxygen species

Zhao

Wen

Wang

et al. 2019

Cell Stress and Chaperones

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Artesunate (ARS) induced significant reactive oxygen species (ROS) generation in HepG2, HeLa, and A549 lines. However, ARS induced ROS-dependent apoptosis in HeLa and A549 cell lines but ROS-independent apoptosis in HepG2 cells. A total of 200 μM hydrogen peroxide (H 2 O 2) significantly induced cytotoxicity in HeLa cells, while H 2 O 2 up to 300 μM did not induce cytotoxicity in HepG2 cells, further demonstrating the strong resistance of HepG2 cells to ROS. HeLa cells had much higher basic total glutathione (T-GSH) level than HepG2 cells, while the ratio of basic reduced glutathione (GSH)/oxidized glutathione (GSSG) in HepG2 cells was nearly twice than that in HeLa and A549 cells. Inhibition of glutathione markedly enhanced H 2 O 2-or ARS-induced cytotoxicity in HeLa and A549 cell lines but modestly enhanced the cytotoxicity of H 2 O 2 and even did not affect the cytotoxicity of ARS in HepG2 cells. Moreover, addition of GSH remarkably prevented H 2 O 2-or ARS-induced cytotoxicity in HeLa and A549 cell lines, further indicating the involvement of GSH in scavenging ROS in the two cell lines. HepG2 cells exhibited higher catalase activity than HeLa cells, and inhibiting catalase activity by using 3-aminotriazole (3-AT, a specific inhibition of catalase) or catalase siRNA remarkably reduced the resistance of HepG2 cells to ROS, demonstrating the key roles of catalase for the strong resistance of HepG2 cells to ROS. Collectively, catalase activity instead of glutathione level dominates the resistance of cells to ROS.

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Dominant roles of Fenton reaction in sodium nitroprusside-induced chondrocyte apoptosis

Cited by 25 publications

References 57 publications

Peroxynitrite dominates sodium nitroprusside-induced apoptosis in human hepatocellular carcinoma cells

Peroxynitrite dominates sodium nitroprusside-induced apoptosis in human hepatocellular carcinoma cells

Role of ATP5G3 in sodium nitroprusside‐induced cell death in cervical carcinoma cells

Intracellular catalase activity instead of glutathione level dominates the resistance of cells to reactive oxygen species

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