Oxidative stress in experimental hepatic steatosis

2001 ◽  
Vol 120 (5) ◽  
pp. A546-A547
Author(s):  
Claudia Pms Oliveria ◽  
Luis Costa Gayotto ◽  
Mariano Janiszewski ◽  
Fabio Pinatel Lopasso ◽  
Francisco Rm Laurindo ◽  
...  
2006 ◽  
Vol 23 (1) ◽  
pp. 91-98 ◽  
Author(s):  
D. BONNEFONT-ROUSSELOT ◽  
V. RATZIU ◽  
P. GIRAL ◽  
F. CHARLOTTE ◽  
I. BEUCLER ◽  
...  

2001 ◽  
Vol 281 (5) ◽  
pp. G1135-G1139 ◽  
Author(s):  
Graham Robertson ◽  
Isabelle Leclercq ◽  
Geoffrey C. Farrell

Oxidative stress is present in the liver of humans with steatosis and nonalcoholic steatohepatitis (NASH) and is a plausible mediator of cellular injury, inflammatory recruitment, and fibrogenesis. CYPs 2E1 and 4A are the microsomal oxidases involved with fatty acid oxidation. Both enzymes can reduce molecular oxygen to produce prooxidant species, which, if not countered efficiently by antioxidants, create oxidative stress. In this theme article, we present the evidence that, in the context of hepatic steatosis, CYPs 2E1 and 4A could generate the “second hit” of cellular injury, particularly when antioxidant reserves are depleted, and propose ways in which this could contribute to the pathogenesis of NASH.


2020 ◽  
Vol 65 ◽  
pp. 103726 ◽  
Author(s):  
Matheus Henrique Romão ◽  
Graziele Freitas de Bem ◽  
Izabelle Barcellos Santos ◽  
Ricardo de Andrade Soares ◽  
Dayane Teixeira Ognibene ◽  
...  

Author(s):  
Karilyn E. Sant ◽  
Hadley M. Moreau ◽  
Larissa M. Williams ◽  
Haydee M. Jacobs ◽  
Anna M. Bowsher ◽  
...  

Abstract Mono-2-ethylhexyl phthalate (MEHP) is the primary metabolite of the ubiquitous plasticizer and toxicant, di-2-ethylhexyl phthalate. MEHP exposure has been linked to abnormal development, increased oxidative stress, and metabolic syndrome in vertebrates. Nuclear factor, Erythroid 2 Like 2 (Nrf2), is a transcription factor that regulates gene expression in response to oxidative stress. We investigated the role of Nrf2a in larval steatosis following embryonic exposure to MEHP. Wild-type and nrf2a mutant (m) zebrafish embryos were exposed to 0 or 200 μg/l MEHP from 6 to either 96 (histology) or 120 hours post fertilization (hpf). At 120 hpf, exposures were ceased and fish were maintained in clean conditions until 15 days post fertilization (dpf). At 15 dpf, fish lengths and lipid content were examined, and the expression of genes involved in the antioxidant response and lipid processing was quantified. At 96 hpf, a subset of animals treated with MEHP had vacuolization in the liver. At 15 dpf, deficient Nrf2a signaling attenuated fish length by 7.7%. MEHP exposure increased hepatic steatosis and increased expression of peroxisome proliferator-activated receptor alpha target fabp1a1. Cumulatively, these data indicate that developmental exposure alone to MEHP may increase risk for hepatic steatosis and that Nrf2a does not play a major role in this phenotype.


2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Aein Azarang ◽  
Omid Farshad ◽  
Mohammad Mehdi Ommati ◽  
Akram Jamshidzadeh ◽  
Reza Heidari ◽  
...  

Background. Treating nonalcoholic fatty liver disease (NAFLD) is considered one of the public health priorities in the past decade. So far, probiotics have represented promising results in controlling the signs and symptoms of NAFLD. However, attempts to find the ideal probiotic strain are still ongoing. The present study is designed to find the best strain amongst suitable probiotic strains according to their ability to ameliorate histopathological and oxidative stress biomarkers in hepatic steatosis-induced rats. Methods. Initially, four probiotics species, including Lactobacillus (L.) acidophilus, L. casei, L. reuteri, and Bacillus coagulans, were cultured and prepared as a lyophilized powder for animals. The experiment lasted for fifty days. Initially, hepatic steatosis was induced by excessive ingestion of D-fructose in rats for eight weeks, followed by eight weeks of administering probiotics and D-fructose concurrently. Forty-two six-week-old male rats were alienated to different groups and were supplemented with different probiotics ( 1 ∗ 10 9   CFU in 500 mL drinking water). After eight weeks, blood and liver samples were taken for further evaluation, and plasma and oxidative stress markers corresponding to liver injuries were examined. Results. Administration of probiotics over eight weeks reversed hepatic and blood triglyceride concentration and blood glucose levels. Also, probiotics significantly suppressed markers of oxidative stress in the liver tissue. Conclusions. Although some of the single probiotic formulations were able to mitigate oxidative stress markers, mixtures of probiotics significantly ameliorated more symptoms in the NAFLD animals. This enhanced effect might be due to probiotics’ cumulative potential to maintain oxidative stress and deliver improved lipid profiles, liver function markers, and inflammatory markers.


2012 ◽  
Vol 287 (48) ◽  
pp. 40732-40744 ◽  
Author(s):  
Miguel A. Lanaspa ◽  
Laura G. Sanchez-Lozada ◽  
Yea-Jin Choi ◽  
Christina Cicerchi ◽  
Mehmet Kanbay ◽  
...  

2009 ◽  
Vol 102 (12) ◽  
pp. 1767-1775 ◽  
Author(s):  
Feral Ozturk ◽  
Mehmet Gul ◽  
Burhan Ates ◽  
I. Cetin Ozturk ◽  
Asli Cetin ◽  
...  

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n42) were divided into six groups of seven each, as follows: control group; CCl4group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4injections were applied to the CCl4groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (β-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.


FEBS Open Bio ◽  
2014 ◽  
Vol 4 (1) ◽  
pp. 522-532 ◽  
Author(s):  
Yoshitaka Kondo ◽  
Hirofumi Masutomi ◽  
Yoshihiro Noda ◽  
Yusuke Ozawa ◽  
Keita Takahashi ◽  
...  

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