Lipid hydroperoxide‐induced apoptosis in human colonic CaCo‐2 cells is associated with an early loss of cellular redox balance

2000 ◽  
Vol 14 (11) ◽  
pp. 1567-1576 ◽  
Author(s):  
Tong‐Gang Wang ◽  
Yudai Gotoh ◽  
Merilyn Ho Jennings ◽  
Carol Ann Rhoads ◽  
Tak Yee Aw
Keyword(s):  
Lipid Hydroperoxide ◽  
Redox Balance ◽  
Cellular Redox ◽  
Early Loss ◽  
Induced Apoptosis

scholarly journals Differential Expression of Peroxisomal Proteins in Distinct Types of Parotid Gland Tumors

2021 ◽  
Vol 22 (15) ◽  
pp. 7872
Author(s):  
Malin Tordis Meyer ◽  
Christoph Watermann ◽  
Thomas Dreyer ◽  
Steffen Wagner ◽  
Claus Wittekindt ◽  
...  
Keyword(s):  
Redox Balance ◽  
Matrix Proteins ◽  
Parotid Tumor ◽  
Gene Expressions ◽  
Tissue Samples ◽  
Cellular Redox ◽  
Tumor Subtypes ◽  
Parotid Tumors ◽  
Aggressive Tumors

Salivary gland cancers are rare but aggressive tumors that have poor prognosis and lack effective cure. Of those, parotid tumors constitute the majority. Functioning as metabolic machinery contributing to cellular redox balance, peroxisomes have emerged as crucial players in tumorigenesis. Studies on murine and human cells have examined the role of peroxisomes in carcinogenesis with conflicting results. These studies either examined the consequences of altered peroxisomal proliferators or compared their expression in healthy and neoplastic tissues. None, however, examined such differences exclusively in human parotid tissue or extended comparison to peroxisomal proteins and their associated gene expressions. Therefore, we examined differences in peroxisomal dynamics in parotid tumors of different morphologies. Using immunofluorescence and quantitative PCR, we compared the expression levels of key peroxisomal enzymes and proliferators in healthy and neoplastic parotid tissue samples. Three parotid tumor subtypes were examined: pleomorphic adenoma, mucoepidermoid carcinoma and acinic cell carcinoma. We observed higher expression of peroxisomal matrix proteins in neoplastic samples with exceptional down regulation of certain enzymes; however, the degree of expression varied between tumor subtypes. Our findings confirm previous experimental results on other organ tissues and suggest peroxisomes as possible therapeutic targets or markers in all or certain subtypes of parotid neoplasms.

scholarly journals Cisplatin inhibits SIRT3-deacetylation MTHFD2 to disturb cellular redox balance in colorectal cancer cell

2020 ◽  
Vol 11 (8) ◽  
Author(s):  
Xingyou Wan ◽  
Chao Wang ◽  
Zhenyu Huang ◽  
Dejian Zhou ◽  
Sheng Xiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Redox Balance ◽  
Colorectal Cancer Cell ◽  
Cellular Redox

scholarly journals A standardized extract of Asparagus officinalis stem improves HSP70-mediated redox balance and cell functions in bovine cumulus-granulosa cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Khoi Thieu Ho ◽  
Kohei Homma ◽  
Jun Takanari ◽  
Hanako Bai ◽  
Manabu Kawahara ◽  
...  
Keyword(s):  
Cell Function ◽  
Redox Balance ◽  
Asparagus Officinalis ◽  
Hsp70 Expression ◽  
Ros Generation ◽  
Cellular Redox ◽  
Pheochromocytoma Cells ◽  
Cell Functions ◽  
Progesterone Synthesis ◽  
Hsp70 Induction

AbstractHeat shock (HS) protein 70 (HSP70), a well-known HS-induced protein, acts as an intracellular chaperone to protect cells against stress conditions. Although HS induces HSP70 expression to confer stress resistance to cells, HS causes cell toxicity by increasing reactive oxygen species (ROS) levels. Recently, a standardized extract of Asparagus officinalis stem (EAS), produced from the byproduct of asparagus, has been shown to induce HSP70 expression without HS and regulate cellular redox balance in pheochromocytoma cells. However, the effects of EAS on reproductive cell function remain unknown. Here, we investigated the effect of EAS on HSP70 induction and oxidative redox balance in cultured bovine cumulus-granulosa (CG) cells. EAS significantly increased HSP70 expression; however, no effect was observed on HSP27 and HSP90 under non-HS conditions. EAS decreased ROS generation and DNA damage and increased glutathione (GSH) synthesis under both non-HS and HS conditions. Moreover, EAS synergistically increased HSP70 and HSF1 expression and increased progesterone levels in CG cells. Treatment with an HSP70 inhibitor significantly decreased GSH level, increased ROS level, and decreased HSF1, Nrf2, and Keap1 expression in the presence of EAS. Furthermore, EAS significantly increased progesterone synthesis. Thus, EAS improves HSP70-mediated redox balance and cell function in bovine CG cells.

scholarly journals NOV-002, a Glutathione Disulfide Mimetic, as a Modulator of Cellular Redox Balance

2008 ◽  
Vol 68 (8) ◽  
pp. 2870-2877 ◽  
Author(s):  
D. M. Townsend ◽  
L. He ◽  
S. Hutchens ◽  
T. E. Garrett ◽  
C. J. Pazoles ◽  
...  
Keyword(s):  
Redox Balance ◽  
Glutathione Disulfide ◽  
Cellular Redox

scholarly journals N-Acetylcysteine as Modulator of the Essential Trace Elements Copper and Zinc

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1117
Author(s):  
Theresa Wolfram ◽  
Maria Schwarz ◽  
Michaela Reuß ◽  
Kristina Lossow ◽  
Mario Ost ◽  
...  
Keyword(s):  
Trace Elements ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Cellular Redox ◽  
Essential Trace Elements ◽  
Nrf2 Activation ◽  
Zn And Cu In ◽  
Cu And Zn

N-acetylcysteine (NAC) is a frequently prescribed drug and known for its metal chelating capability. However, to date it is not well characterized whether NAC intake affects the homeostasis of essential trace elements. As a precursor of glutathione (GSH), NAC also has the potential to modulate the cellular redox homeostasis. Thus, we aimed to analyze effects of acute and chronic NAC treatment on the homeostasis of copper (Cu) and zinc (Zn) and on the activity of the redox-sensitive transcription factor Nrf2. Cells were exposed to 1 mM NAC and were co-treated with 50 μM Cu or Zn. We showed that NAC treatment reduced the cellular concentration of Zn and Cu. In addition, NAC inhibited the Zn-induced Nrf2 activation and limited the concomitant upregulation of cellular GSH concentrations. In contrast, mice chronically received NAC via drinking water (1 g NAC/100 mL). Cu and Zn concentrations were decreased in liver and spleen. In the duodenum, NQO1, TXNRD, and SOD activities were upregulated by NAC. All of them can be induced by Nrf2, thus indicating a putative Nrf2 activation. Overall, NAC modulates the homeostasis of Cu and Zn both in vitro and in vivo and accordingly affects the cellular redox balance.

scholarly journals Betula etnensis Raf. (Betulaceae) Extract Induced HO-1 Expression and Ferroptosis Cell Death in Human Colon Cancer Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 2723 ◽  
Author(s):  
Giuseppe Antonio Malfa ◽  
Barbara Tomasello ◽  
Rosaria Acquaviva ◽  
Carlo Genovese ◽  
Alfonsina La Mantia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Death ◽  
Cell Viability ◽  
Lipid Hydroperoxide ◽  
Human Colon ◽  
Redox Status ◽  
Heme Oxygenase 1 ◽  
Human Colon Cancer ◽  
Cellular Redox

Betula etnensis Raf. (Birch Etna) belonging to the Betulaceae family grows on the eastern slope of Etna. Many bioactive compounds present in Betula species are considered promising anticancer agents. In this study, we evaluated the effects of B. etnensis Raf. bark methanolic extract on a human colon cancer cell line (CaCo2). In order to elucidate the mechanisms of action of the extract, cellular redox status, cell cycle, and heme oxygenase-1 (HO-1) expression in ferroptosis induction were evaluated. Cell viability and proliferation were tested by tetrazolium (MTT) assayand cell cycle analysis, while cell death was evaluated by annexin V test and lactic dehydrogenase (LDH) release. Cellular redox status was assessed by measuring thiol groups (RSH) content, reactive oxygen species (ROS) production, lipid hydroperoxide (LOOH) levels and (γ-glutamylcysteine synthetase) γ-GCS and HO-1 expressions. The extract significantly reduced cell viability of CaCo2, inducing necrotic cell death in a concentration-depending manner. In addition, an increase in ROS levels and a decrease of RSH content without modulation in γ-GCS expression were detected, with an augmentation in LOOH levels and drastic increase in HO-1 expression. These results suggest that the B. etnensis Raf. extract promotes an oxidative cellular microenvironment resulting in CaCo2 cell death by ferroptosis mediated by HO-1 hyper-expression.

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