Involvement of vertebrate hemoglobin in antioxidant protection: chicken blood as a model

2007 ◽  
Vol 85 (3) ◽  
pp. 404-412 ◽  
Author(s):  
Alcir Luiz Dafre ◽  
Tiago A.S. Brandão ◽  
Evaldo Reischl
Keyword(s):  
Redox Balance ◽  
Evolutionary Trend ◽  
Cellular Redox ◽  
Reactive Protein ◽  
Cellular Events ◽  
Protein Thiols ◽  
Antioxidant Function ◽  
Chicken Erythrocytes ◽  
Redox Buffer ◽  
Chicken Blood

Redox balance can be described as the equilibrium between oxidative and reductive forces within the cell. These forces control several cellular events, including the modulation of redox-sensitive receptors and signaling pathways. In cells, glutathione is the major non-protein thiol and is considered the main redox buffer. The ratio between the oxidized (GSSG) and reduced (GSH) forms reflects the cellular redox balance. Reactive protein thiols, including vertebrate hemoglobin (Hb), have been proposed as effective antioxidants that can contribute to the redox balance. To further explore this possibility, chicken ( Gallus gallus (L., 1758)) blood was used as a model system. The use of known oxidants (hydroperoxides, diamide, and a system generating reactive oxygen species) originated a pattern of glutathiolation in chicken erythrocytes that was fully reversed after removal of the oxidant, this being consistent with a physiological response. The glutathiolation sequence correlates to kinetic data on chicken Hb cysteine reactivity. The major chicken hemoglobin (Hb A) is responsible for most of the glutathiolated protein where the presence of externally positioned and fast-reacting cysteines is a contributing factor. The antioxidant potential of fast-reacting Hb cysteines is in line with the conservation of cysteine residues in Hb stereochemical positions in more than 95% of the available avian Hb sequences. This may represent an evolutionary trend for the antioxidant function of externally positioned and reactive cysteines in abundant proteins.

scholarly journals The SP/NK1R System-Mediated ROS Generation in GBM Cells through Inhibiting Glutaredoxin Protein

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Negeen Mehrabani ◽  
Mohammad Reza Vaezi Kakhki ◽  
Hossein Javid ◽  
Safieh Ebrahimi ◽  
Seyed Isaac Hashemy
Keyword(s):  
Redox Balance ◽  
Ros Generation ◽  
Contributing Factors ◽  
Cellular Redox ◽  
Redox Active ◽  
Resazurin Assay ◽  
Intracellular Ros ◽  
Polymerase Chain ◽  
Neurokinin 1 ◽  
Redox Buffer

Altered redox balance is among the main contributing factors developing glioblastoma multiforme (GBM), a highly aggressive grade IV brain tumor. Neuropeptide substance P (SP) plays a key role in modifying the cellular redox environment by activating the neurokinin-1 receptor (NK1R). In this study, we aimed to investigate the redox-modulating properties of both SP and a commercially available NK1R antagonist, aprepitant in GBM cells. To detect the effect of aprepitant on the viability of U87 glioblastoma cells, resazurin assay was applied. The level of intracellular ROS was assessed using 2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA) assay. The expression of glutaredoxin, a well-known redox-active protein, was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Concurrently, the activity of glutaredoxin was also analyzed by a commercial kit (ZellBio GmbH). We found that SP increased the intracellular levels of reactive oxygen species (ROS) in U87 GBM cells, and aprepitant remarkably decreased this effect. We also explored the effects of SP/NK1R signaling on the glutaredoxin system as a major cellular redox buffer in GBM cells. SP reduced both expression and enzymatic activity of glutaredoxin, and these effects were significantly decreased by aprepitant. In conclusion, our results suggest a possible involvement of SP/NK1R signaling in GBM pathogenesis through oxidative stress and offering new insight for the application of aprepitant as a redox-modulating strategy in GBM patients.

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

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 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.

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