Ochratoxin A induces karyomegaly and cell cycle aberrations in renal tubular cells without relation to induction of oxidative stress responses in rats

2014 ◽  
Vol 224 (1) ◽  
pp. 64-72 ◽  
Author(s):  
Eriko Taniai ◽  
Atsunori Yafune ◽  
Masahiro Nakajima ◽  
Shim-Mo Hayashi ◽  
Fumiyuki Nakane ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Ochratoxin A ◽  
Stress Responses ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Oxidative Stress Responses

scholarly journals BMP7 reduces inflammation and oxidative stress in diabetic tubulopathy

2014 ◽  
Vol 128 (4) ◽  
pp. 269-280 ◽  
Author(s):  
Rui Xi Li ◽  
Wai Han Yiu ◽  
Hao Jia Wu ◽  
Dickson W. L. Wong ◽  
Loretta Y. Y. Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Advanced Glycation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Glycation End Products ◽  
Renal Tubular ◽  
Diabetic Tubulopathy ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

BMP7 ameliorates diabetic tubulopathy by suppressing inflammatory and oxidative stress responses both in cultured renal tubular cells exposed to advanced glycation end-products and in diabetic db/db mice.

scholarly journals Classification of Five Uremic Solutes according to Their Effects on Renal Tubular Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Takeo Edamatsu ◽  
Ayako Fujieda ◽  
Atsuko Ezawa ◽  
Yoshiharu Itoh
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Viable Cell ◽  
Cell Number ◽  
Viable Cell Number ◽  
Cycle Progression ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Uremic Solutes ◽  
Renal Tubular

Background/Aims. Uremic solutes, which are known to be retained in patients with chronic kidney disease, are considered to have deleterious effects on disease progression. Among these uremic solutes, indoxyl sulfate (IS) has been extensively studied, while other solutes have been studied less to state. We conducted a comparative study to examine the similarities and differences between IS,p-cresyl sulfate (PCS), phenyl sulfate (PhS), hippuric acid (HA), and indoleacetic acid (IAA).Methods. We used LLC-PK1 cells to evaluate the effects of these solutes on viable cell number, cell cycle progression, and cell death.Results. All the solutes reduced viable cell number after 48-hour incubation. N-Acetyl-L-cysteine inhibited this effect induced by all solutes except HA. At the concentration that reduced the cell number to almost 50% of vehicle control, IAA induced apoptosis but not cell cycle delay, whereas other solutes induced delay in cell cycle progression with marginal impact on apoptosis. Phosphorylation of p53 and Chk1 and expression of ATF4 and CHOP genes were detected in IS-, PCS-, and PhS-treated cells, but not in IAA-treated cells.Conclusions. Taken together, the adverse effects of PCS and PhS on renal tubular cells are similar to those of IS, while those of HA and IAA differ.

scholarly journals Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing oxidative stress-mediated cell death pathways

2015 ◽  
Vol 12 (4) ◽  
pp. 6086-6092 ◽  
Author(s):  
TSAI-KUN WU ◽  
CHYOU-WEI WEI ◽  
YING-RU PAN ◽  
SHUR-HUEIH CHERNG ◽  
WEI-JUNG CHANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Vitamin C ◽  
Toxic Effect ◽  
Aristolochic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Cell Death Pathways ◽  
Renal Tubular

Reduction of Oxidative Stress in Cultured Renal Tubular Cells and Preventive Effects on Renal Stone Formation by the Bioflavonoid Quercetin

2008 ◽  
Vol 179 (4) ◽  
pp. 1620-1626 ◽  
Author(s):  
Hyoung Keun Park ◽  
Byong Chang Jeong ◽  
Mi-Kyung Sung ◽  
Mi-Young Park ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Preventive Effects

Prolonged K + deficiency increases intracellular ATP, cell cycle arrest and cell death in renal tubular cells

Metabolism ◽  
2017 ◽  
Vol 74 ◽  
pp. 47-61 ◽  
Author(s):  
Kedsarin Fong-ngern ◽  
Nardtaya Ausakunpipat ◽  
Nilubon Singhto ◽  
Kanyarat Sueksakit ◽  
Visith Thongboonkerd
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Intracellular Atp ◽  
Cycle Arrest ◽  
K Deficiency ◽  
Renal Tubular

Examination of the anti-oxidative effect in renal tubular cells and apoptosis by oxidative stress

2005 ◽  
Vol 33 (4) ◽  
pp. 261-266 ◽  
Author(s):  
Yasunori Itoh ◽  
Takahiro Yasui ◽  
Atsushi Okada ◽  
Keiichi Tozawa ◽  
Yutaro Hayashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Oxidative Effect

scholarly journals Nox4 has a crucial role in uric acid-induced oxidative stress and apoptosis in renal tubular cells

2016 ◽  
Vol 13 (5) ◽  
pp. 4343-4348 ◽  
Author(s):  
Zhuohang Li ◽  
Yiyu Sheng ◽  
Cheng Liu ◽  
Kuiqing Li ◽  
Xin Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Crucial Role ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Xuezhong Gong ◽  
Yiru Duan ◽  
Junli Zheng ◽  
Yiquan Wang ◽  
Guohua Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Contrast Induced Nephropathy ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
P38 Mapk Pathway ◽  
Thioredoxin 1 ◽  
Renal Tubular

Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI) due to apoptosis induced in renal tubular cells. Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro. In the present study, we aimed to compare the efficacies of NACA and NAC in preventing CIN in a well-established rat model and investigate whether thioredoxin-1 (Trx1) and apoptosis signal-regulating kinase 1 (ASK1) act as the potential activator for p38 MAPK. NACA significantly attenuated elevations of serum creatinine, blood urea nitrogen, and biomarkers of AKI. At equimolar concentration, NACA was more effective than NAC in reducing histological changes of renal tubular injuries. NACA attenuated activation of p38 MAPK signal, reduced oxidative stress, and diminished apoptosis. Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC. To our knowledge, this is the first report that Trx1 and ASK1 are involved in CIN. Our study highlights a renal protective role of NACA against CIN through modulating Trx1 and ASK1/p38 MAPK pathway to result in the inhibition of apoptosis among renal cells.

Sign in / Sign up

Export Citation Format

Share Document