The Role of ROS and RNS in Regulating Life and Death of Blood Monocytes

Baran, Christopher P.; Zeigler, Mandy M.; Tridandapani, Susheela; Marsh, Clay B.

doi:10.2174/1381612043452866

Cited by 135 publications

(101 citation statements)

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“…• OH) regulate many essential cellular events such as gene expression, differentiation, cell proliferation and cell death (1). A change in the redox state of tissues and cells affects an alteration in the generation or metabolism of ROS.…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide induces human pulmonary fibroblast cell death via increasing ROS levels and GSH depletion

You

Park

2012

Oncology Reports

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Abstract. Arsenic trioxide (ATO; As 2 O 3 ) induces apoptotic cell death in various cancer cells including lung cancer via the induction of reactive oxygen species (ROS). However, little is known about the toxicological effects of ATO on normal primary lung cells. Here, we investigated the effects of N-acetyl cysteine (NAC) and vitamin C (well-known antioxidants) or L-buthionine sulfoximine (BSO; an inhibitor of GSH synthesis) on ATO-treated human pulmonary fibroblast (HPF) cells in relation to cell death, ROS and glutathione (GSH). ATO induced growth inhibition and death in HPF cells, accompanied by the loss of mitochondrial membrane potential (MMP; ∆Ψ m ). ATO increased ROS levels including O 2•-and GSH depleted cell numbers. NAC attenuated the growth inhibition, death and MMP (∆Ψ m ) loss in ATO-treated HPF cells and also decreased the ROS levels in these cells. However, vitamin C enhanced the growth inhibition, death, MMP (∆Ψ m ) loss and GSH depletion by ATO and even strongly increased mitochondrial O 2•-levels in ATO-treated HPF cells. BSO showed a strong increase in ROS levels in ATO-treated HPF cells and intensified the growth inhibition, cell death, MMP (∆Ψ m ) loss and GSH depletion. Moreover, superoxide dismutase (SOD2) or thioredoxin (TXN) siRNAs attenuated HPF cell death by ATO, which was not correlated with ROS and GSH level changes. In conclusion, ATO induced the growth inhibition and death of HPF cells, accompanied by increasing ROS levels and GSH depletion. NAC attenuated HPF cell death by ATO whereas vitamin C and BSO enhanced the death.

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Section: Introductionmentioning

confidence: 99%

Arsenic trioxide induces human pulmonary fibroblast cell death via increasing ROS levels and GSH depletion

You

Park

2012

Oncology Reports

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“…These molecules regulate many important cellular events, including transcription factor activation, gene expression, differentiation, and cell proliferation (1,2). ROS are formed as by-products of mitochondrial respiration or the action of oxidases, including nicotine adenine diphosphate (NADPH) oxidase, xanthine oxidase (XO) and certain arachidonic acid oxygenases (3).…”

Section: Introductionmentioning

confidence: 99%

The effects of N-acetyl cysteine, buthionine sulfoximine, diethyldithiocarbamate or 3-amino-1,2,4-triazole on antimycin A-treated Calu-6 lung cells in relation to cell growth, reactive oxygen species and glutathione

Park¹

2009

Oncol Rep

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Abstract. Antimycin A (AMA) inhibits mitochondrial electron transport between cytochrome b and c. We recently demonstrated that AMA inhibits the growth of lung cancer Calu-6 cells and the changes of reactive oxygen species (ROS) and glutathione (GSH) levels affect apoptosis in Calu-6 cells. Here, we examined the effects of N-acetylcysteine (NAC, a well known antioxidant), L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyldithiocarbamate (DDC, an inhibitor of Cu, Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on AMAtreated Calu-6 cells in relation to cell death, ROS and GSH levels. Treatment with AMA induced cell growth inhibition, apoptosis and the loss of mitochondrial membrane potential (MMP) (Δae m ) in Calu-6 cells. While the intracellular ROS level was decreased in 50 μM AMA-treated Calu-6 cells, O 2•-levels among ROS were significantly increased. AMA also induced GSH depletion in Calu-6 cells. Treatment with NAC showed decreasing effect on O 2•-levels in AMA-treated cells preventing apoptosis, MMP (Δae m ) loss and GSH depletion in these cells. BSO significantly increased GSH depletion and apoptosis in AMA-treated cells. While both DDC and AT increased ROS levels in AMA-treated Calu-6 cells, only DDC intensified GSH depletion and apoptosis. BSO and AT increased the ROS level in Calu-6 control cells, but these agents did not induce apoptosis and GSH depletion. In conclusion, our results suggest that GSH depletion rather than ROS level in AMA-treated Calu-6 cells is more tightly related to apoptosis.

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“…They have recently been implicated in the regulation of many important cellular events, including transcription factor activation, gene expression, differentiation and proliferation (1)(2)(3). ROS are formed as by-products of mitochondrial respiration or oxidases including nicotine adenine diphosphate (NADPH) oxidase, xanthine oxidase (XO) and certain arachidonic acid oxygenases (4).…”

Section: Introductionmentioning

confidence: 99%

Pyrogallol as a glutathione depletorinduces apoptosis in HeLa cells

Han

Kim²,

Kim³

et al. 2008

Int J Mol Med

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Abstract. Pyrogallol, a polyphenol, is known to be a superoxide anion (O 2 •-) generator. We investigated the involvement of glutathione (GSH) and reactive oxygen species (ROS) in pyrogallol-induced HeLa cell death. We measured the changes of ROS levels, GSH levels, sub-G1 cells, annexin V/PI staining cells and mitochondria membrane potential (ΔΨ m ) in HeLa cells treated with pyrogallol and/or ROS scavenger. The intracellular ROS levels were decreased or increased depending on the concentration of pyrogallol. The level of O 2•-was significantly increased and superoxide dismutase (SOD) activity was down-regulated by pyrogallol. Pyrogallol reduced intracellular GSH content in HeLa cells. The ROS scavengers, Tempol, Tiron, Trimetazidine and N-acetylcysteine (NAC), did not down-regulate the production of O 2•-. However, treatment with NAC showed the recovery of GSH depletion and significantly rescued cells from pyrogallolinduced apoptosis. In addition, the recovery of GSH depletion by SOD and catalase was accompanied by the decrease of apoptosis levels. Furthermore, NAC and SOD significantly inhibited CMF-negative (GSH-depleted) and PI-positive cells induced by pyrogallol. Taken together, pyrogallol potently increased intracellular O 2•-levels and decreased GSH content in HeLa cells, and NAC, SOD and catalase significantly rescued HeLa cells from pyrogallol-induced apoptosis accompanied by the recovery of GSH depletion.

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The Role of ROS and RNS in Regulating Life and Death of Blood Monocytes

Cited by 135 publications

References 0 publications

Arsenic trioxide induces human pulmonary fibroblast cell death via increasing ROS levels and GSH depletion

Arsenic trioxide induces human pulmonary fibroblast cell death via increasing ROS levels and GSH depletion

The effects of N-acetyl cysteine, buthionine sulfoximine, diethyldithiocarbamate or 3-amino-1,2,4-triazole on antimycin A-treated Calu-6 lung cells in relation to cell growth, reactive oxygen species and glutathione

Pyrogallol as a glutathione depletorinduces apoptosis in HeLa cells

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