scholarly journals Liver injury in acute fatty liver of pregnancy: Possible link to placental mitochondrial dysfunction and oxidative stress

Hepatology ◽  
2009 ◽  
Vol 51 (1) ◽  
pp. 191-200 ◽  
Author(s):  
Sathish Kumar Natarajan ◽  
Kavitha R. Thangaraj ◽  
C. E. Eapen ◽  
Anup Ramachandran ◽  
Ashis Mukhopadhya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Fatty Liver ◽  
Mitochondrial Dysfunction ◽  
Acute Fatty Liver ◽  
And Oxidative Stress

scholarly journals Acute fatty liver of pregnancy: an update on mechanisms

2011 ◽  
Vol 4 (3) ◽  
pp. 99-103 ◽  
Author(s):  
Sathish Kumar Natarajan ◽  
Kavitha R Thangaraj ◽  
Ashish Goel ◽  
C E Eapen ◽  
K A Balasubramanian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Maternal Circulation ◽  
Subcellular Organelles ◽  
Microvesicular Steatosis ◽  
Acute Fatty Liver ◽  
And Oxidative Stress

Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis.

scholarly journals Minocycline Decreases Liver Injury after Hemorrhagic Shock and Resuscitation in Mice

HPB Surgery ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Christoph Czerny ◽  
Andaleb Kholmukhamedov ◽  
Tom P. Theruvath ◽  
Eduardo N. Maldonado ◽  
Venkat K. Ramshesh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Mitochondrial Dysfunction ◽  
Intravital Microscopy ◽  
Caspase 3 ◽  
Multiple Organ ◽  
Shed Blood ◽  
Lactated Ringer's Solution ◽  
Liver Homogenates ◽  
And Oxidative Stress

Patients that survive hemorrhage and resuscitation (H/R) may develop a systemic inflammatory response syndrome (SIRS) that leads to dysfunction of vital organs (multiple organ dysfunction syndrome, MODS). SIRS and MODS may involve mitochondrial dysfunction. Under pentobarbital anesthesia, C57BL6 mice were hemorrhaged to 30 mm Hg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer’s solution containing minocycline, tetracycline (both 10 mg/kg body weight) or vehicle. Serum alanine aminotransferase (ALT), necrosis, apoptosis and oxidative stress were assessed 6 h after resuscitation. Mitochondrial polarization was assessed by intravital microscopy. After H/R with vehicle or tetracycline, ALT increased to 4538 U/L and 3999 U/L, respectively, which minocycline decreased to 1763 U/L (P<0.01). Necrosis and TUNEL also decreased from 24.5% and 17.7 cells/field, respectively, after vehicle to 8.3% and 8.7 cells/field after minocycline. Tetracycline failed to decrease necrosis (23.3%) but decreased apoptosis to 9 cells/field (P<0.05). Minocycline and tetracycline also decreased caspase-3 activity in liver homogenates. Minocycline but not tetracycline decreased lipid peroxidation after resuscitation by 70% (P<0.05). Intravital microscopy showed that minocycline preserved mitochondrial polarization after H/R (P<0.05). In conclusion, minocycline decreases liver injury and oxidative stress after H/R by preventing mitochondrial dysfunction.

scholarly journals Capybara Oil Improves Hepatic Mitochondrial Dysfunction, Steatosis, and Inflammation in a Murine Model of Nonalcoholic Fatty Liver Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Polyana C. Marinho ◽  
Aline B. Vieira ◽  
Priscila G. Pereira ◽  
Kíssila Rabelo ◽  
Bianca T. Ciambarella ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Mitochondrial Dysfunction ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Positive Effects ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is recognized as the most common cause of liver dysfunction worldwide and is commonly associated with obesity. Evidences suggest that NAFLD might be a mitochondrial disease, which contributes to the hepatic steatosis, oxidative stress, cytokine release, and cell death. Capybara oil (CO) is a rich source of polyunsaturated fatty acids (PUFA), which is known to improve inflammation and oxidative stress. In order to determine the effects of CO on NAFLD, C57Bl/6 mice were divided into 3 groups and fed a high-fat diet (HFD) (NAFLD group and NAFLD + CO group) or a control diet (CG group) during 16 weeks. The CO (1.5 g/kg/daily) was administered by gavage during the last 4 weeks of the diet protocol. We evaluated plasma liver enzymes, hepatic steatosis, and cytokine expression in liver as well as hepatocyte ultrastructural morphology and mitochondrial function. CO treatment suppressed hepatic steatosis, attenuated inflammatory response, and decreased plasma alanine aminotransferase (ALT) in mice with NAFLD. CO was also capable of restoring mitochondrial ultrastructure and function as well as balance superoxide dismutase and catalase levels. Our findings indicate that CO treatment has positive effects on NAFLD improving mitochondrial dysfunction, steatosis, acute inflammation, and oxidative stress.

scholarly journals Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

2008 ◽  
Vol 44 (7) ◽  
pp. 1259-1272 ◽  
Author(s):  
Sudheer K. Mantena ◽  
Adrienne L. King ◽  
Kelly K. Andringa ◽  
Heather B. Eccleston ◽  
Shannon M. Bailey
Keyword(s):  
Oxidative Stress ◽  
Fatty Liver ◽  
Mitochondrial Dysfunction ◽  
Liver Diseases ◽  
And Oxidative Stress

scholarly journals Autophagy mitigates ethanol-induced mitochondrial dysfunction and oxidative stress in esophageal keratinocytes

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0239625
Author(s):  
Prasanna M. Chandramouleeswaran ◽  
Manti Guha ◽  
Masataka Shimonosono ◽  
Kelly A. Whelan ◽  
Hisatsugu Maekawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress

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.

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