Acute ethanol preexposure promotes liver regeneration after partial hepatectomy in mice by activating ALDH2

It is known that chronic ethanol significantly impairs liver regeneration. However, the effect of acute ethanol exposure on liver regeneration remains largely unknown. To address this question, C57Bl6/J mice were exposed to acute ethanol (6 g/kg intragastrically) for 3 days, and partial hepatectomy (PHx) was performed 24 h after the last dose. Surprisingly, acute ethanol preexposure promoted liver regeneration. This effect of ethanol did not correlate with changes in expression of cell cycle regulatory genes (e.g., cyclin D1, p21, and p27) but did correlate with protection against the effect of PHx on indices of impaired lipid and carbohydrate metabolism. Ethanol preexposure protected against inhibition of the oxidant-sensitive mitochondrial enzyme, aconitase. The activity of aldehyde dehydrogenase 2 (ALDH2) was significantly increased by ethanol preexposure. The effect of ethanol was blocked by inhibiting (Daidzin) and was mimicked by activating (Alda-1) ALDH2. Lipid peroxides are also substrates for ALDH2; indeed, alcohol preexposure blunted the increase in lipid peroxidation (4OH-nonenal adducts) caused by PHx. Taken together, these data suggest that acute preoperative ethanol exposure “preconditions” the liver to respond more rapidly to regenerate after PHx by activating mitochondrial ALDH2, which prevents oxidative stress in this compartment.

Download Full-text

Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl4administration

Hepatology ◽

10.1002/hep.510240331 ◽

1996 ◽

Vol 24 (3) ◽

pp. 657-662 ◽

Cited By ~ 61

Author(s):

I Aguilar-Delfin ◽

F López-Barrera ◽

R Hernández-Munoz

Keyword(s):

Lipid Peroxidation ◽

Plasma Membrane ◽

Liver Regeneration ◽

Partial Hepatectomy ◽

Experimental Models ◽

Selective Enhancement

Download Full-text

Effect of vitamin C on liver regeneration after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats

International Surgery Journal ◽

10.18203/2349-2902.isj20210358 ◽

2021 ◽

Vol 8 (2) ◽

pp. 489

Author(s):

Reno Rudiman ◽

Handy Wing ◽

Nurhayat Usman

Keyword(s):

Lipid Peroxidation ◽

Liver Injury ◽

Vitamin C ◽

Liver Regeneration ◽

Partial Hepatectomy ◽

Wistar Rats ◽

Liver Weight ◽

Potential Effect ◽

Regeneration Rate ◽

Male Wistar Rats

Background: The aim of this study is to evaluate the potential effect of vitamin C as an antioxidant on liver regeneration after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats.Methods: A total of 24 male Wistar rats were divided into four groups, each group consisted of 6 rats: group A (control, partial hepatectomy/PHx alone), group B (PHx and vitamin C 250 mg/kg BW), group C (acetaminophen 500 mg/kg BW and PHx), and group D (acetaminophen 500 mg/kg BW with PHx and vitamin C 250 mg/kg BW). Subtoxic dose of acetaminophen was given 24 hours before partial hepatectomy. Vitamin C was given orally via oral gavage for 6 consecutive days after partial hepatectomy. POD 7, all animals were terminated and performed laparotomy to obtain liver tissue for measurement of liver weight and regeneration rate, blood samples for malondialdehyde (MDA) as a lipid peroxidation measurement and histopathological investigation.Results: The means of regeneration rate in vitamin C groups were significantly higher compared to non-vitamin C group (p<0.05). Similar result, the means of MDA values in vitamin C groups were significantly lower compared to non-vitamin C group (p<0.05). This result suggests a protective effect of vitamin C against lipid peroxidation. Histopathological changes in liver cells were statistically difference between vitamin C groups and non-vitamin C groups (p<0.05).Conclusions: Our results indicate that vitamin C administration promotes liver regeneration and inhibits lipid peroxidation after partial hepatectomy and acetaminophen-induced liver injury in Wistar rats.

Download Full-text

Bevacizumab Allows Preservation of Liver Function and its Regenerative Capacity after Major Hepatectomy

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666190417162409 ◽

2019 ◽

Vol 19 (11) ◽

pp. 1388-1398

Author(s):

Amparo Valverde ◽

Rubén Ciria ◽

Javier Caballero-Villarraso ◽

Patricia Aguilar-Melero ◽

Gustavo Ferrín ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Liver Regeneration ◽

Major Hepatectomy ◽

High Dose ◽

Histopathological Analysis ◽

Liver Resections ◽

Tnf Α ◽

Toxicity Analysis ◽

The Impact

Background: Parallel to the safety of liver resections, new chemotherapy drugs have emerged for the control of liver metastases. However, there is unclear evidence about the combination of intensive BVZ-therapy and extended resections. The main aim was to analyse the impact of Bevacizumab (BVZ) in terms of liver safety and tolerability in two experimental models: a basal-toxicity situation and after major hepatectomy. Methods: Eighty male-Wistar rats were grouped as toxicity analysis (sham-operated rats-OS-) and regenerationafter- surgery analysis (hepatectomy rats-H-). Eight further subgroups were created according to sacrifice (6- hours-6h- or 24-hours-24h-) and dose (μg) of BVZ (none, 100, 200, 400). Several measurements were performed, including biochemical serum samples, histopathological analysis, cytokines (IL-6, TNF-α, TGF-β), oxidative-stress (GSH/GSSG, ATP), lipid-peroxidation (TBARS) and epidermal and vascular endothelium growth-factors (EGF and VEGF). Results: In the toxicity analysis, safe results with BVZ were observed, with no significant differences among the groups. A trend towards a lower oxidative status was observed in the OS 6 h-100, -200 and -400 versus the OS 6 h-none group. Similar results were observed in the hepatectomy model, with stable oxidative-stress-index and IL-6, TNF- α, and TGF- β levels. Despite higher lipid peroxidation status, overall regeneration was preserved. As expected, VEGF was almost undetectable in BVZ-treated groups after resection, but not in the non-resection group. Conclusion: It was concluded that liver status was not impaired by BVZ even at the high-dose. Similarly, liver regeneration after extended hepatectomy in BVZ-treated animals was well-preserved. Extended liver resections may be encouraged in BVZ-treated patients due to its excellent tolerability and good liver regeneration status.

Download Full-text

Myocardial Oxidative Stress and Toxicity Induced by Acute Ethanol Exposure in Mice

Experimental Biology and Medicine ◽

10.1177/153537020422900614 ◽

2004 ◽

Vol 229 (6) ◽

pp. 553-559 ◽

Cited By ~ 55

Author(s):

Muralidhar Kannan ◽

Lipeng Wang ◽

Y. James Kang

Keyword(s):

Oxidative Stress ◽

Ethanol Exposure ◽

Myocardial Oxidative Stress ◽

Acute Ethanol

Download Full-text

p38α deficiency restrains liver regeneration after partial hepatectomy triggering oxidative stress and liver injury

Scientific Reports ◽

10.1038/s41598-019-39428-3 ◽

2019 ◽

Vol 9 (1) ◽

Author(s):

Sergio Rius-Pérez ◽

Ana M. Tormos ◽

Salvador Pérez ◽

Isabela Finamor ◽

Patricia Rada ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Liver Regeneration ◽

Partial Hepatectomy

Download Full-text

Taurine prevents enhancement of acetylcholinesterase activity induced by acute ethanol exposure and decreases the level of markers of oxidative stress in zebrafish brain

Neuroscience ◽

10.1016/j.neuroscience.2010.09.030 ◽

2010 ◽

Vol 171 (3) ◽

pp. 683-692 ◽

Cited By ~ 75

Author(s):

D.B. Rosemberg ◽

R.F. da Rocha ◽

E.P. Rico ◽

A. Zanotto-Filho ◽

R.D. Dias ◽

...

Keyword(s):

Oxidative Stress ◽

Acetylcholinesterase Activity ◽

Ethanol Exposure ◽

Zebrafish Brain ◽

Acute Ethanol ◽

Markers Of Oxidative Stress

Download Full-text

Babao Dan attenuates acute ethanol-induced liver injury via Nrf2 activation and autophagy

Cell & Bioscience ◽

10.1186/s13578-019-0343-6 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 3

Author(s):

Yang Yu ◽

Zhi-qiang Tian ◽

Lei Liang ◽

Xue Yang ◽

Dan-dan Sheng ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Sleep Time ◽

Ethanol Exposure ◽

Related Factor ◽

Glutamate Cysteine Ligase ◽

Nrf2 Activation ◽

Acute Ethanol ◽

Hepatic Lipid Peroxidation ◽

Hepatic Cytochrome

Abstract Background Babao Dan (BBD), a traditional Chinese medicine, has been used as a complementary and alternative medicine to treat multifarious liver diseases. In this study, we aimed to observe its protective effect on ethanol-induced liver injury and explore potential mechanisms. Methods Mice pretreated with BBD (0.125, 0.25 and 0.5 g/kg BW) were administrated by ethanol gavage (5 g/kg BW). Liver injury biomarkers and hepatic redox parameters were evaluated by histopathology as well as serum and hepatic content analysis. AML-12 cell was also utilized to determine the efficacy of BBD against ethanol-induced hepatotoxicity. Results Drunkenness experiment showed that the latency was significantly increased and the drunken sleep time was decreased in mice pretreated with BBD. We then found that BBD could reduce hepatic lipid peroxidation and steatosis induced by ethanol exposure. BBD could also suppress ethanol-induced depletion of hepatic antioxidant enzyme. Besides that, BBD treatment lessened the induction of hepatic cytochrome P450 2E1, a major contributor to ethanol-mediated oxidative stress, and up-regulated the expression of nuclear factor erythroid 2-related factor 2 and its two transcriptional targets hemeoxygenase-1 and glutamate-cysteine ligase catalytic subunit. Furthermore, autophagy induced by BBD contributed to hepatoprotection activity. Conclusions Our results suggest that BBD can markedly dispel acute ethanol-induced hepatotoxicity through multiple pathways including attenuation of ethanol-mediated oxidative stress, enhancement of the oxidative defense systems and activation of autophagy.

Download Full-text

Lipid peroxidation is not a prerequisite for the development of obesity and diabetes in high-fat-fed mice

British Journal Of Nutrition ◽

10.1017/s0007114508191243 ◽

2009 ◽

Vol 102 (3) ◽

pp. 462-469 ◽

Cited By ~ 21

Author(s):

Florence M. Sohet ◽

Audrey M. Neyrinck ◽

Evelyne M. Dewulf ◽

Laure B. Bindels ◽

Laurence Portois ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Metabolic Response ◽

Lipid Peroxides ◽

Thiobarbituric Acid ◽

Chow Diet ◽

High Fat ◽

High Concentration ◽

Adipose Tissues ◽

Obesity And Diabetes

The mechanism, by which a high-fat (HF) diet could impair glucose metabolism, is not completely understood but could be related to inflammation, lipotoxicity and oxidative stress. Lipid peroxides have been proposed as key mediators of intracellular metabolic response. The purpose of the present study was to analyse, in mice fed with a HF diet, the possible association between obesity and glucose tolerance on the one hand, and between oxidative stress and lipid peroxidation on the other hand. The present results show that a HF diet (70 % energy as fat), v. a high-carbohydrate chow diet (control), increases body weight and fat mass development, and impairs glycaemia and insulinaemia within 4 weeks. It also promotes the expression of NADPH oxidase in the liver – signing both oxidative and inflammatory stress – but decreases thiobarbituric acid-reactive substances content in the liver as well as in epididymal, subcutaneous and visceral adipose tissues. HF diet, with elevated vitamin E content, induces high concentration of α-tocopherol in liver and adipose tissues, which contributes to the protection against lipid peroxidation. Thus, lipid peroxidation in key organs is not necessarily related to the development of metabolic disorders associated with diabetes and obesity.

Download Full-text

Products of Lipid Peroxidation as a Factor in the Toxic Effect of Silver Nanoparticles

Materials ◽

10.3390/ma13112460 ◽

2020 ◽

Vol 13 (11) ◽

pp. 2460 ◽

Cited By ~ 1

Author(s):

Patrycja Paciorek ◽

Mariusz Żuberek ◽

Agnieszka Grzelak

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Silver Nanoparticles ◽

Energy Metabolism ◽

Cell Viability ◽

Toxic Effect ◽

Lipid Peroxides ◽

Cellular Lipid ◽

Amino Groups ◽

Lipid Peroxidation Products

In our previous study we have shown that nanoparticles have different effects depending on the energy metabolism of the cell, which is an important factor in the context of oncology and diabetes. Here we assess the influence of AgNPs on cellular lipid components in varying glucose concentrations. To assess the effect of silver nanoparticles on cell lipids, we measured cell viability, the fluidity of the cell membranes, the content of amino groups in proteins, the level of lipid peroxidation products, the concentration of 4-hydroxynonenal (4-HNE), and the concentration of lipid peroxides. The obtained results show differences in the formation of lipid peroxidation products in cells exposed to oxidative stress induced by nanoparticles. In addition, we have shown that the metabolic state of the cell is a factor significantly affecting this process.

Download Full-text