scholarly journals Protective effect of carnosine on hydrogen peroxide–induced oxidative stress in human kidney tubular epithelial cells

2021 ◽  
Vol 534 ◽  
pp. 576-582
Author(s):  
Yadi Cao ◽  
Juan Xu ◽  
Di Cui ◽  
Lei Liu ◽  
Shiqi Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Protective Effect ◽  
Human Kidney ◽  
Tubular Epithelial Cells

scholarly journals Oxalate-induced activation of PKC-α and -δ regulates NADPH oxidase-mediated oxidative injury in renal tubular epithelial cells

2009 ◽  
Vol 297 (5) ◽  
pp. F1399-F1410 ◽  
Author(s):  
Vijayalakshmi Thamilselvan ◽  
Mani Menon ◽  
Sivagnanam Thamilselvan
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Cell Injury ◽  
Oxidative Injury ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Ldh Release ◽  
Renal Tubular

Oxalate-induced oxidative stress contributes to cell injury and promotes renal deposition of calcium oxalate crystals. However, we do not know how oxalate stimulates reactive oxygen species (ROS) in renal tubular epithelial cells. We investigated the signaling mechanism of oxalate-induced ROS formation in these cells and found that oxalate significantly increased membrane-associated protein kinase C (PKC) activity while at the same time lowering cytosolic PKC activity. Oxalate markedly translocated PKC-α and -δ from the cytosol to the cell membrane. Pretreatment of LLC-PK1cells with specific inhibitors of PKC-α or -δ significantly blocked oxalate-induced generation of superoxide and hydrogen peroxide along with NADPH oxidase activity, LDH release, lipid hydroperoxide formation, and apoptosis. The PKC activator PMA mimicked oxalate's effect on oxidative stress in LLC-PK1cells as well as cytosol-to-membrane translocation of PKC-α and -δ. Silencing of PKC-α expression by PKC-α-specific small interfering RNA significantly attenuated oxalate-induced cell injury by decreasing hydrogen peroxide generation and LDH release. We believe this is the first demonstration that PKC-α- and -δ-dependent activation of NADPH oxidase is one of the mechanisms responsible for oxalate-induced oxidative injury in renal tubular epithelial cells. The study suggests that the therapeutic approach might be considered toward attenuating oxalate-induced PKC signaling-mediated oxidative injury in recurrent stone formers.

scholarly journals Underlying Histopathology Determines Response to Oxidative Stress in Cultured Human Primary Proximal Tubular Epithelial Cells

2020 ◽  
Vol 21 (2) ◽  
pp. 560
Author(s):  
Muhammad Ali Khan ◽  
Xiangju Wang ◽  
Kurt T.K. Giuliani ◽  
Purba Nag ◽  
Anca Grivei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Epithelial Cells ◽  
Functional Response ◽  
Mitochondrial Function ◽  
Human Kidney ◽  
Tubular Epithelial Cells ◽  
Cortical Tissue ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular

Proximal tubular epithelial cells (PTEC) are key players in the progression of kidney diseases. PTEC studies to date have primarily used mouse models and transformed human PTEC lines. However, the translatability of these models to human kidney disease has been questioned. In this study, we investigated the phenotypic and functional response of human primary PTEC to oxidative stress, an established driver of kidney disease. Furthermore, we examined the functional contribution of the underlying histopathology of the cortical tissue used to generate our PTEC. We demonstrated that human primary PTEC from both histologically ‘normal’ and ‘diseased’ cortical tissue responded to H2O2-induced oxidative stress with significantly elevated mitochondrial superoxide levels, DNA damage, and significantly decreased proliferation. The functional response of ‘normal’ PTEC to oxidative stress mirrored the reported pathogenesis of human kidney disease, with significantly attenuated mitochondrial function and increased cell death. In contrast, ‘diseased’ PTEC were functionally resistant to oxidative stress, with maintenance of mitochondrial function and cell viability. This selective survival of ‘diseased’ PTEC under oxidizing conditions is reminiscent of the in vivo persistence of maladaptive PTEC following kidney injury. We are now exploring the impact that these differential PTEC responses have in the therapeutic targeting of oxidative stress pathways.

scholarly journals Protective effect of vanillic acid in hydrogen peroxide-induced oxidative stress in D.Mel-2 cell line

2020 ◽  
Author(s):  
Shagufta Taqvi ◽  
Eijaz Ahmed Bhat ◽  
Nasreena Sajjad ◽  
Jamal S.M. Sabir ◽  
Aleem Qureshi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Cell Line ◽  
Vanillic Acid

Tubular epithelial cells have the capacity to transdifferentiate into CD68-positive macrophage-like cells by oxidative stress

2008 ◽  
Vol 57 (12) ◽  
pp. 593-600 ◽  
Author(s):  
M. Tanaka ◽  
Y. Suzuki ◽  
I. Shirato ◽  
H. Takahara ◽  
T. Shibata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Tubular Epithelial Cells

scholarly journals Caffeic Acid - Potential Antioxidant in Cultured Human Retinal Pigment Epithelial Cells

1970 ◽  
Vol 66 (2) ◽  
Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Caffeic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Defence ◽  
Rpe Cells ◽  
In Cells

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.

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