Hesperidin protects against the chlorpyrifos‐induced chronic hepato‐renal toxicity in rats associated with oxidative stress, inflammation, apoptosis, autophagy, and up‐regulation of PARP ‐1 / VEGF

2021 ◽  
Author(s):  
Sefa Küçükler ◽  
Selim Çomaklı ◽  
Selçuk Özdemir ◽  
Cüneyt Çağlayan ◽  
Fatih Mehmet Kandemir
Keyword(s):  
Oxidative Stress ◽  
Renal Toxicity ◽  
Parp 1

scholarly journals Cancer Imprints an Increased PARP-1 and p53-Dependent Resistance to Oxidative Stress on Lymphocytes of Patients That Later Develop Alzheimer's Disease

2018 ◽  
Vol 12 ◽  
Author(s):  
Felipe Salech ◽  
Daniela P. Ponce ◽  
Carol D. SanMartín ◽  
Nicole K. Rogers ◽  
Mauricio Henríquez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Parp 1

Toxicoproteomic Analysis of Poly(ADP-Ribose)-Associated Proteins Induced by Oxidative Stress in Human Proximal Tubule Cells

2019 ◽  
Vol 171 (1) ◽  
pp. 117-131
Author(s):  
Argel Islas-Robles ◽  
Deepthi Yedlapudi ◽  
Serrine S Lau ◽  
Terrence J Monks
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Proximal Tubule ◽  
Calcium Influx ◽  
Regulation Of Transcription ◽  
Loss Of Function ◽  
Proximal Tubule Cells ◽  
Associated Proteins ◽  
Tubule Cells ◽  
Parp 1

Abstract 2,3,5-Tris-(glutathion-S-yl)hydroquinone (TGHQ) is a nephrotoxic and nephrocarcinogenic metabolite of hydroquinone. TGHQ generates reactive oxygen species (ROS), causing DNA-strand breaks, hyperactivation of PARP-1, increases in intracellular calcium ([Ca2+]i), and cell death. PARP-1 catalyzes the attachment of ADP-ribose polymers (PAR) to target proteins. In human kidney proximal tubule cells, ROS-mediated PARP-1 hyperactivation and elevations in [Ca2+]i are reciprocally coupled. The molecular mechanism of this interaction is unclear. The aim of the present study was to identify ROS-induced PAR-associated proteins to further understand their potential role in cell death. PAR-associated proteins were enriched by immunoprecipitation, identified by LC-MS/MS, and relative abundance was obtained by spectral counting. A total of 356 proteins were PAR-modified following TGHQ treatment. A total of 13 proteins exhibited gene ontology annotations related to calcium. Among these proteins, the general transcription factor II-I (TFII-I) is directly involved in the modulation of [Ca2+]i. TFII-I binding to phospholipase C (PLC) leads to calcium influx via the TRPC3 channel. However, inhibition of TRPC3 or PLC had no effect on TGHQ-mediated cell death, suggesting that their loss of function may be necessary but insufficient to cause cell death. Nevertheless, TGHQ promoted a time-dependent translocation of TFII-I from the nucleus to the cytosol concomitant with a decrease in tyrosine phosphorylation in α/β-TFII-I. Therefore it is likely that ROS have an important impact on the function of TFII-I, such as regulation of transcription, and DNA translesion synthesis. Our data also shed light on PAR-mediated signaling during oxidative stress, and contributes to the development of strategies to prevent PAR-dependent cell death.

scholarly journals Protective effect of essential oil of Cinnamomum verum bark on hepatic and renal toxicity induced by carbon tetrachloride in rats

2019 ◽  
Vol 44 (6) ◽  
pp. 606-618 ◽  
Author(s):  
Khaled Bellassoued ◽  
Ferdaws Ghrab ◽  
Houda Hamed ◽  
Rim Kallel ◽  
Jos van Pelt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Renal Toxicity ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Untreated Group ◽  
Protective Effects ◽  
Glutamyl Transferase

The inner bark of cinnamon (Cinnamomum verum) is widely used as a spice. Cinnamon plants are also a valuable source of essential oil used for medicinal purposes. The present study aimed to investigate the composition and in vitro antioxidant activity of essential oil of C. verum bark (CvEO) and its protective effects in vivo on CCl4-induced hepatic and renal toxicity in rats. Groups of animals were pretreated for 7 days with CvEO (70 or 100 mg/kg body weight) or received no treatment and on day 7 a single dose of CCl4 was used to induce oxidative stress. Twenty-four hours after CCl4 administration, the animals were euthanized. In the untreated group, CCl4 induced an increase in serum biochemical parameters and triggered oxidative stress in both liver and kidneys. CvEO (100 mg/kg) caused significant reductions in CCl4-elevated levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyl transferase, lactate dehydrogenase, total cholesterol, triglycerides, low-density lipoprotein, urea, and creatinine and increased the level of high-density lipoprotein compared with the untreated group. Moreover, pretreatment with CvEO at doses of 70 and 100 mg/kg before administration of CCl4 produced significant reductions in thiobarbituric acid reactive substances and protein carbonyl levels in liver and kidney tissues compared with the untreated group. The formation of pathological hepatic and kidney lesions induced by the administration of CCl4 was strongly prevented by CvEO at a dose of 100 mg/kg. Overall, this study suggests that administration of CvEO has high potential to quench free radicals and alleviate CCl4-induced hepatorenal toxicity in rats.

Oxidative stress and renal toxicity after subacute exposure to decabrominated diphenyl ether in Wistar rats

2015 ◽  
Vol 25 (8) ◽  
pp. 7223-7230 ◽  
Author(s):  
Vesna Milovanovic ◽  
Aleksandra Buha ◽  
Vesna Matovic ◽  
Marijana Curcic ◽  
Slavica Vucinic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Renal Toxicity ◽  
Diphenyl Ether ◽  
Subacute Exposure

scholarly journals Loss of Androgen Receptor in Aging and Oxidative Stress through Myb Protooncoprotein-regulated Reciprocal Chromatin Dynamics of p53 and Poly(ADP-ribose) Polymerase PARP-1

2008 ◽  
Vol 283 (52) ◽  
pp. 36474-36485 ◽  
Author(s):  
Liheng Shi ◽  
Soyoung Ko ◽  
Soyoung Kim ◽  
Ibtissam Echchgadda ◽  
Tae-Sung Oh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Androgen Receptor ◽  
Chromatin Dynamics ◽  
Parp 1 ◽  
And Oxidative Stress

scholarly journals Accelerated Aging during Chronic Oxidative Stress: A Role for PARP-1

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Daniëlle M. P. H. J. Boesten ◽  
Joyce M. J. de Vos-Houben ◽  
Leen Timmermans ◽  
Gertjan J. M. den Hartog ◽  
Aalt Bast ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Diseases ◽  
Human Fibroblasts ◽  
Methylation Status ◽  
Accelerated Aging ◽  
Chronic Inflammatory Disease ◽  
Telomere Shortening ◽  
Chronic Oxidative Stress ◽  
Linear Chromosomes ◽  
Parp 1

Oxidative stress plays a major role in the pathophysiology of chronic inflammatory disease and it has also been linked to accelerated telomere shortening. Telomeres are specialized structures at the ends of linear chromosomes that protect these ends from degradation and fusion. Telomeres shorten with each cell division eventually leading to cellular senescence. Research has shown that poly(ADP-ribose) polymerase-1 (PARP-1) and subtelomeric methylation play a role in telomere stability. We hypothesized that PARP-1 plays a role in accelerated aging in chronic inflammatory diseases due to its role as coactivator of NF-κb and AP-1. Therefore we evaluated the effect of chronic PARP-1 inhibition (by fisetin and minocycline) in human fibroblasts (HF) cultured under normal conditions and under conditions of chronic oxidative stress, induced bytert-butyl hydroperoxide (t-BHP). Results showed that PARP-1 inhibition under normal culturing conditions accelerated the rate of telomere shortening. However, under conditions of chronic oxidative stress, PARP-1 inhibition did not show accelerated telomere shortening. We also observed a strong correlation between telomere length and subtelomeric methylation status of HF cells. We conclude that chronic PARP-1 inhibition appears to be beneficial in conditions of chronic oxidative stress but may be detrimental under relatively normal conditions.

Secoisolariciresinol diglucoside protects against cadmium-induced oxidative stress-mediated renal toxicity in rats

2020 ◽  
Vol 61 ◽  
pp. 126552
Author(s):  
Tareq Aqeel ◽  
Sunil Chikkalakshmipura Gurumallu ◽  
Ashwini Bhaskar ◽  
Saeed Mujahid hashimi ◽  
Rajesh Javaraiah
Keyword(s):  
Oxidative Stress ◽  
Renal Toxicity ◽  
Secoisolariciresinol Diglucoside
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