scholarly journals The Effect oftert-Butyl Hydroperoxide-Induced Oxidative Stress on Lean and Steatotic Rat HepatocytesIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Otto Kučera ◽  
René Endlicher ◽  
Tomáš Roušar ◽  
Halka Lotková ◽  
Tomáš Garnol ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Respiratory Control ◽  
Rat Hepatocytes ◽  
Severe Damage ◽  
Total Glutathione ◽  
Nonalcoholic Fatty Liver ◽  
Butyl Hydroperoxide ◽  
Toxic Liver Injury ◽  
Dependent State

Oxidative stress and mitochondrial dysfunction play an important role in the pathogenesis of nonalcoholic fatty liver disease and toxic liver injury. The present study was designed to evaluate the effect of exogenous inducer of oxidative stress (tert-butyl hydroperoxide, tBHP) on nonfatty and steatotic hepatocytes isolated from the liver of rats fed by standard and high-fat diet, respectively. In control steatotic hepatocytes, we found higher generation of ROS, increased lipoperoxidation, an altered redox state of glutathione, and decreased ADP-stimulated respiration using NADH-linked substrates, as compared to intact lean hepatocytes. Fatty hepatocytes exposed to tBHP exert more severe damage, lower reduced glutathione to total glutathione ratio, and higher formation of ROS and production of malondialdehyde and are more susceptible to tBHP-induced decrease in mitochondrial membrane potential. Respiratory control ratio of complex I was significantly reduced by tBHP in both lean and steatotic hepatocytes, but reduction in NADH-dependent state 3 respiration was more severe in fatty cells. In summary, our results collectively indicate that steatotic rat hepatocytes occur under conditions of enhanced oxidative stress and are more sensitive to the exogenous source of oxidative injury. This confirms the hypothesis of steatosis being the first hit sensitizing hepatocytes to further damage.

scholarly journals One Week of CDAHFD Induces Steatohepatitis and Mitochondrial Dysfunction with Oxidative Stress in Liver

2021 ◽  
Vol 22 (11) ◽  
pp. 5851
Author(s):  
Takehito Sugasawa ◽  
Seiko Ono ◽  
Masato Yonamine ◽  
Shin-ichiro Fujita ◽  
Yuki Matsumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Early Stage ◽  
Droplet Deposition ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
Mitochondrial Dna Copy Number ◽  
Short Period ◽  
And Oxidative Stress

The prevalence of nonalcoholic fatty liver disease (NAFLD) has been rapidly increasing worldwide. A choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) has been used to create a mouse model of nonalcoholic steatohepatitis (NASH). There are some reports on the effects on mice of being fed a CDAHFD for long periods of 1 to 3 months. However, the effect of this diet over a short period is unknown. Therefore, we examined the effect of 1-week CDAHFD feeding on the mouse liver. Feeding a CDAHFD diet for only 1-week induced lipid droplet deposition in the liver with increasing activity of liver-derived enzymes in the plasma. On the other hand, it did not induce fibrosis or cirrhosis. Additionally, it was demonstrated that CDAHFD significantly impaired mitochondrial respiration with severe oxidative stress to the liver, which is associated with a decreasing mitochondrial DNA copy number and complex proteins. In the gene expression analysis of the liver, inflammatory and oxidative stress markers were significantly increased by CDAHFD. These results demonstrated that 1 week of feeding CDAHFD to mice induces steatohepatitis with mitochondrial dysfunction and severe oxidative stress, without fibrosis, which can partially mimic the early stage of NASH in humans.

scholarly journals Protective Effects of Saponin Mixture, Isolated from <i>Astragalus monspessulanus</i> subsp. <i>monspessulanus</i> on Tert-Butyl Hydroperoxide—Induced Oxidative Stress in Isolated Rat Hepatocytes

2015 ◽  
Vol 06 (06) ◽  
pp. 799-803 ◽  
Author(s):  
Magdalena Spasova Kondeva-Burdina ◽  
Viktor Bratkov ◽  
Rumyana Lubomirova Simeonova ◽  
Vessela Bisserova Vitcheva ◽  
Ilina Nikolaeva Krasteva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Rat Hepatocytes ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Isolated Rat

Aromatic aldehyde compound cuminaldehyde protects nonalcoholic fatty liver disease in rats feeding high fat diet

2019 ◽  
Vol 38 (7) ◽  
pp. 823-832 ◽  
Author(s):  
MR Haque ◽  
SH Ansari
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Liver Enzymes ◽  
Liver Weight ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is caused by fat accumulation and is related with obesity and oxidative stress. In this study, we investigated the effect of cuminaldehyde on NAFLD in rats fed a high fat diet (HFD). Male Wistar rats were fed a HFD for 42 days to induce NAFLD. The progression of NAFLD was evaluated by histology and measuring liver enzymes (alanine transaminase and aspartate transaminase), serum and hepatic lipids (total triglycerides and total cholesterol), and oxidative stress markers (thiobarbituric acid reactive substances, glutathione, superoxide dismutase, and catalase). The HFD feeding increased the liver weight and caused NAFLD, liver steatosis, hyperlipidemia, oxidative stress, and elevated liver enzymes. Administration of cuminaldehyde ameliorated the changes in hepatic morphology and liver weight, decreased levels of liver enzymes, and inhibited lipogenesis. Our findings suggest that cuminaldehyde could improve HFD-induced NAFLD via abolishment of hepatic oxidative damage and hyperlipidemia. Cuminaldehyde might be considered as a potential aromatic compound in the treatment of NAFLD and obesity through the modulation of lipid metabolism.

scholarly journals CYP2J2 overexpression attenuates nonalcoholic fatty liver disease induced by high-fat diet in mice

2015 ◽  
Vol 308 (2) ◽  
pp. E97-E110 ◽  
Author(s):  
Guangzhi Chen ◽  
Renfan Xu ◽  
Shasha Zhang ◽  
Yinna Wang ◽  
Peihua Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Jnk Signaling ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress

Cytochrome P-450 epoxygenase-derived epoxyeicosatrienoic acids (EETs) exert diverse biological activities, which include potent vasodilatory, anti-inflammatory, antiapoptotic, and antioxidatant effects, and cardiovascular protection. Liver has abundant epoxygenase expression and high levels of EET production; however, the roles of epoxygenases in liver diseases remain to be elucidated. In this study, we investigated the protection against high-fat diet-induced nonalcoholic fatty liver disease (NAFLD) in mice with endothelial-specific CYP2J2 overexpression (Tie2-CYP2J2-Tr). After 24 wk of high-fat diet, Tie2-CYP2J2-Tr mice displayed attenuated NAFLD compared with controls. Tie2-CYP2J2-Tr mice showed significantly decreased plasma triglyceride levels and liver lipid accumulation, improved liver function, reduced inflammatory responses, and less increase in hepatic oxidative stress than wild-type control mice. These effects were associated with inhibition of NF-κB/JNK signaling pathway activation and enhancement of the antioxidant defense system in Tie2-CYP2J2-Tr mice in vivo. We also demonstrated that 14,15-EET treatment protected HepG2 cells against palmitic acid-induced inflammation and oxidative stress. 14,15-EET attenuated palmitic acid-induced changes in NF-κB/JNK signaling pathways, malondialdehyde generation, glutathione levels, reactive oxygen species production, and NADPH oxidase and antioxidant enzyme expression in HepG2 cells in vitro. Together, these results highlight a new role for CYP epoxygenase-derived EETs in lipotoxicity-related inflammation and oxidative stress and reveal a new molecular mechanism underlying EETs-mediated anti-inflammatory and antioxidant effects that could aid in the design of new therapies for the prevention and treatment of NAFLD.

scholarly journals One Week Feeding of CDAHFD Induces Steatohepatitis and Mitochondrial Dysfunction with Oxidative Stress in Liver

2021 ◽  
Author(s):  
Takehito Sugasawa ◽  
Seiko Ono ◽  
Masato Yonanine ◽  
Shin-ichiro Fujita ◽  
Yuki Matsumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Early Stage ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
Mitochondrial Dna Copy Number ◽  
Short Period ◽  
Long Time ◽  
And Oxidative Stress

The prevalence of nonalcoholic fatty liver disease (NAFLD) has been rapidly increasing worldwide. A choline-deficient L-amino acid-defined high fat diet (CDHFD) has been used to create a mouse model of nonalcoholic steatohepatitis (NASH). There are some reports about the effects on mice of being fed CDAHFD for a long time, 1 to 3 months. However, the effect of this diet over a short period has been unknown. Therefore, we examined the effect of one week of feeding CDAHFD on the mouse liver. Feeding this diet for only one week induced lipid droplet deposition in the liver with increasing activity of liver-derived enzymes in the plasma. On the other hand, it did not induce fibrosis and cirrhosis. Additionally, it was demonstrated that mitochondrial respiration is significantly impaired with severe oxidative stress in the liver by CDAHFD, associated with a decreasing mitochondrial DNA copy number and complexes-proteins. In the gene expression analysis of the liver, inflammatory and oxidative stress markers were significantly increased by CDAHFD. These results demonstrated that one week of feeding CDAHFD to mice induces steatohepatitis with mitochondrial dysfunction and severe oxidative stress, without fibrosis, which can partially mimic the early stage of the NASH in humans.

scholarly journals Attenuation of High-Fat Diet-Induced Rat Liver Oxidative Stress and Steatosis by Combined Hydroxytyrosol- (HT-) Eicosapentaenoic Acid Supplementation Mainly Relies on HT

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Francisca Echeverría ◽  
Rodrigo Valenzuela ◽  
Andrés Bustamante ◽  
Daniela Álvarez ◽  
Macarena Ortiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Eicosapentaenoic Acid ◽  
High Fat Diet ◽  
Control Diet ◽  
Liver Steatosis ◽  
Pharmacological Therapy ◽  
High Fat ◽  
Total Recovery ◽  
Nonalcoholic Fatty Liver ◽  
The Impact

Pharmacological therapy for nonalcoholic fatty liver disease (NAFLD) is not approved at the present time. For this purpose, the effect of combined eicosapentaenoic acid (EPA; 50 mg/kg/day) modulating hepatic lipid metabolism and hydroxytyrosol (HT; 5 mg/kg/day) exerting antioxidant actions was evaluated on hepatic steatosis and oxidative stress induced by a high-fat diet (HFD; 60% fat, 20% protein, and 20% carbohydrates) compared to a control diet (CD; 10% fat, 20% protein, and 70% carbohydrates) in mice fed for 12 weeks. HFD-induced liver steatosis (i) was reduced by 32% by EPA, without changes in oxidative stress-related parameters and mild recovery of Nrf2 functioning affording antioxidation and (ii) was decreased by 42% by HT, concomitantly with total regain of the glutathione status diminished by HFD, 42% to 59% recovery of lipid peroxidation and protein oxidation enhanced by HFD, and regain of Nrf2 functioning, whereas (iii) combined EPA + HT supplementation elicited 74% reduction in liver steatosis, with total recovery of the antioxidant potential in a similar manner than HT. It is concluded that combined HT + EPA drastically decreases NAFLD development, an effect that shows additivity in HT and EPA effects that mainly relies on HT, strengthening the impact of oxidative stress as a central mechanism underlying liver steatosis in obesity.

Antioxidative properties of natural coelenterazine and synthetic methyl coelenterazine in rat hepatocytes subjected to tert-butyl hydroperoxide-induced oxidative stress

2000 ◽  
Vol 60 (4) ◽  
pp. 471-478 ◽  
Author(s):  
Marlène L.N Dubuisson ◽  
Bertrand de Wergifosse ◽  
André Trouet ◽  
Fernand Baguet ◽  
Jacqueline Marchand-Brynaert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Hepatocytes ◽  
Butyl Hydroperoxide ◽  
Antioxidative Properties ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

High-fat diet stimulates hepatic cystathionine β-synthase and cystathionine γ-lyase expression

2013 ◽  
Vol 91 (11) ◽  
pp. 913-919 ◽  
Author(s):  
Sun-Young Hwang ◽  
Lindsei K. Sarna ◽  
Yaw L. Siow ◽  
Karmin O
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Lipid Peroxides ◽  
High Fat ◽  
Significant Elevation ◽  
Total Glutathione ◽  
Protein Levels ◽  
Adaptive Role

Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) catalyze homocysteine (Hcy) metabolism via the trans-sulfuration pathway. They are also responsible for hydrogen sulfide (H2S) production via desulfuration reactions. The liver contributes significantly to the regulation of Hcy and H2S homeostasis, which might participate in many physiological and pathological processes. The aim of this study was to investigate the effect of a high-fat diet (HFD) on hepatic CBS and CSE expression and its impact on Hcy and H2S metabolism. Mice (C57BL/6) fed a HFD (60% kcal fat) for 5 weeks developed fatty liver. The mRNA and protein levels of CBS and CSE in the liver were significantly elevated in mice fed a HFD. Subsequently the metabolism of Hcy by CBS and CSE was increased in the liver, and its level decreased in the circulation. Increased CBS and CSE expression also caused a significant elevation in H2S production in the liver. The level of lipid peroxides was elevated, indicating oxidative stress, while the level of total glutathione remained unchanged in the liver of HFD-fed mice. Upregulation of the trans-sulfuration pathway might play an adaptive role against oxidative stress by maintaining total glutathione levels in the liver.

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