scholarly journals Epigallocatechin-3-Gallate Reduces Hepatic Oxidative Stress and Lowers CYP-Mediated Bioactivation and Toxicity of Acetaminophen in Rats

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1862 ◽  
Author(s):  
Hsien-Tsung Yao ◽  
Chien-Chun Li ◽  
Chen-Hui Chang
Keyword(s):  
Oxidative Stress ◽  
Organic Anion ◽  
Antioxidant Enzyme Activity ◽  
Organic Anion Transporting Polypeptides ◽  
Histological Changes ◽  
Egcg Treatment ◽  
Hepatic Oxidative Stress ◽  
Cyp 1A2 ◽  
Induced Apoptosis ◽  
Alanine Aminotransferase Activity

Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol in green tea. To investigate the effects of dietary EGCG on oxidative stress and the metabolism and toxicity of acetaminophen in the liver, rats were fed diets with (0.54%) or without EGCG supplementation for four weeks and were then injected intraperitoneally with acetaminophen (1 g/kg). The results showed that EGCG lowered hepatic oxidative stress and cytochrome P450 (CYP) 1A2, 2E1, and 3A, and UDP-glucurosyltransferase activities prior to acetaminophen injection. After acetaminophen challenge, the elevations in plasma alanine aminotransferase activity and histological changes in the liver were ameliorated by EGCG treatment. EGCG reduced acetaminophen-induced apoptosis by lowering the Bax/Bcl2 ratio in the liver. EGCG mildly increased autophagy by increasing the LC3B II/I ratio. Lower hepatic acetaminophen–glutathione and acetaminophen–protein adducts contents were observed after EGCG treatment. EGCG increased glutathione peroxidase and NAD(P)H quinone 1 oxidoreductase activities and reduced organic anion-transporting polypeptides 1a1 expression in the liver after acetaminophen treatment. Our results indicate that EGCG may reduce oxidative stress and lower the metabolism and toxicity of acetaminophen. The reductions in CYP-mediated acetaminophen bioactivation and uptake transporter, as well as enhanced antioxidant enzyme activity, may limit the accumulation of toxic products in the liver and thus lower hepatotoxicity.

scholarly journals Deltamethrin Induces Apoptosis in Cerebrum Neurons of Quail via Promoting Endoplasmic Reticulum Stress and Mitochondrial Dysfunction

2021 ◽  
Author(s):  
Pengfei Wu ◽  
Bing Han ◽  
Qingyue Yang ◽  
Siyu Li ◽  
Xiaoqiao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Chronic Exposure ◽  
Molecular Mechanisms ◽  
Atp Content ◽  
Histological Changes ◽  
Real Time Quantitative Pcr ◽  
Induced Apoptosis

Abstract Deltamethrin (DLM) is a widely used and highly effective insecticide. DLM exposure is harmful to animal and human. Quail, as a bird model, has been widely used in the toxicology field. However, there is little information available in the literature about quail cerebrum damage caused by DLM. Here, we investigated the effect of DLM on quail cerebrum neurons. Four groups of healthy quails were assigned (10 quails in each group), respectively given 0, 15, 30, and 45 mg/kg DLM by gavage for 12 weeks. Through the measurements of quail cerebrum, it was found that DLM exposure induced obvious histological changes, oxidative stress, and neurons apoptosis. To further explore the possible molecular mechanisms, we performed real-time quantitative PCR to detect the expression of endoplasmic reticulum (ER) stress-related mRNA. In addition, we detected ATP content in quail cerebrum to evaluate the functional status of mitochondria. The study showed that DLM exposure significantly increased the expression of ER stress-related mRNA and decreased ATP content in quail cerebrum. These results suggest that chronic exposure to DLM induces apoptosis of quail cerebrum neurons via promoting ER stress and mitochondrial dysfunction. Furthermore, our results provide a novel explanation for DLM-induced apoptosis of avian cerebrum neurons.

scholarly journals Quercetin Effects on Hepatotoxicity Induced by Titanium Dioxide Nanoparticles in Rats

2019 ◽  
Vol 15 (3) ◽  
Author(s):  
Maryam Shirani ◽  
Layasadat Khorsandi ◽  
Hadis Alidadi
Keyword(s):  
Oxidative Stress ◽  
Titanium Dioxide ◽  
Wistar Rats ◽  
Titanium Dioxide Nanoparticles ◽  
Serum Biomarker ◽  
Histological Changes ◽  
Nuclear Pyknosis ◽  
Female Wistar Rats ◽  
Body Organ ◽  
Induced Apoptosis

Background: Most nanoparticles have adverse impacts on the liver, which is a vital body organ, by the induction of oxidative stress. Objectives: This study was designed to evaluate the hepatoprotective effects of quercetin (QCT) against the toxicity of nanoscale titanium dioxide (NTiO2) in Wistar rats. Methods: The present study was conducted on 32 adult female Wistar rats assigned into 4 groups of control, NTiO2 (50 mg/kg), NTiO2 + Quercetin (50 + 75 mg/kg), and Quercetin (75 mg/kg). The animals exposed to NTiO2 were administered by 50 mg/kg of NTiO2 for 21 days. The Quercetin + NTiO2 rats received Quercetin before exposing to NTiO2 for 7 days. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) of serum were considered indicators of the hepatotoxicity. The oxidative stress was assessed by measuring the activity of catalase (CAT) and superoxide dismutase (SOD) as well as the level of malondialdehyde (MDA) in the liver. TUNEL assay and histological changes were also assessed. Results: The NTiO2 significantly elevated the MDA level (P < 0.01), enhanced the serum biomarker levels, reduced the CAT (P < 0.01) and SOD (P < 0.01) activities. The NTiO2 also aggregated the red blood cells, and caused inflammatory cell infiltration, nuclear pyknosis and fat deposit in hepatocytes, as well as induced apoptosis in the liver tissue. Pretreatment with QCT quenched oxidative stress, attenuated the histological changes, elevated the CAT (P < 0.01) and SOD (P < 0.01) activities, normalized the serum biomarker levels and decreased apoptosis (P < 0.001). Conclusions: The QCT has an inhibitory impact on hepatotoxicity induced by nanoparticles in rats.

scholarly journals Effect of oxidative stress on expression and function of human and rat organic anion transporting polypeptides in the liver

2013 ◽  
Vol 458 (2) ◽  
pp. 262-271 ◽  
Author(s):  
Takashi Tsujimoto ◽  
Jiro Ogura ◽  
Kaori Kuwayama ◽  
Takahiro Koizumi ◽  
Shunichi Sasaki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Organic Anion ◽  
Organic Anion Transporting Polypeptides ◽  
And Function

Cocoa flavonoids up-regulate antioxidant enzyme activity via the ERK1/2 pathway to protect against oxidative stress-induced apoptosis in HepG2 cells☆

2010 ◽  
Vol 21 (3) ◽  
pp. 196-205 ◽  
Author(s):  
María Ángeles Martín ◽  
Ana Belén Granado Serrano ◽  
Sonia Ramos ◽  
María Izquierdo Pulido ◽  
Laura Bravo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Antioxidant Enzyme ◽  
Hepg2 Cells ◽  
Antioxidant Enzyme Activity ◽  
Induced Apoptosis

Black Tea-Induced Amelioration of Hepatic Oxidative Stress through Antioxidative Activity in EAC-Bearing Mice

2007 ◽  
Vol 26 (4) ◽  
pp. 245-254 ◽  
Author(s):  
Arindam Bhattacharyya ◽  
Debaprasad Mandal ◽  
Lakshmishri Lahiry ◽  
Sankar Bhattacharyya ◽  
Sreya Chattopadhyay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidative Activity ◽  
Black Tea ◽  
Hepatic Oxidative Stress ◽  
Induced Amelioration

Hybrid Compounds & Oxidative Stress Induced Apoptosis in Cancer Therapy

2020 ◽  
Vol 27 (13) ◽  
pp. 2118-2132 ◽  
Author(s):  
Aysegul Hanikoglu ◽  
Hakan Ozben ◽  
Ferhat Hanikoglu ◽  
Tomris Ozben
Keyword(s):  
Oxidative Stress ◽  
Drug Resistance ◽  
Side Effects ◽  
Cancer Therapy ◽  
Tumor Cells ◽  
Anticancer Drugs ◽  
Chemotherapeutic Agents ◽  
Oxidation Reactions ◽  
Hybrid Compounds ◽  
Induced Apoptosis

: Elevated Reactive Oxygen Species (ROS) generated by the conventional cancer therapies and the endogenous production of ROS have been observed in various types of cancers. In contrast to the harmful effects of oxidative stress in different pathologies other than cancer, ROS can speed anti-tumorigenic signaling and cause apoptosis of tumor cells via oxidative stress as demonstrated in several studies. The primary actions of antioxidants in cells are to provide a redox balance between reduction-oxidation reactions. Antioxidants in tumor cells can scavenge excess ROS, causing resistance to ROS induced apoptosis. Various chemotherapeutic drugs, in their clinical use, have evoked drug resistance and serious side effects. Consequently, drugs having single-targets are not able to provide an effective cancer therapy. Recently, developed hybrid anticancer drugs promise great therapeutic advantages due to their capacity to overcome the limitations encountered with conventional chemotherapeutic agents. Hybrid compounds have advantages in comparison to the single cancer drugs which have usually low solubility, adverse side effects, and drug resistance. This review addresses two important treatments strategies in cancer therapy: oxidative stress induced apoptosis and hybrid anticancer drugs.

Excessive Oxidative Stress in the Synergistic Effects of Shikonin on the Hyperthermia-Induced Apoptosis

2018 ◽  
Vol 18 (5) ◽  
pp. 322-334 ◽  
Author(s):  
J.-L. Piao ◽  
Y.-J. Jin ◽  
M.-L. Li ◽  
S.A. Zakki ◽  
L. Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synergistic Effects ◽  
Induced Apoptosis
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