scholarly journals Boldine Supplementation Regulates Mitochondrial Function and Oxidative Stress in a Rat Model of Hepatotoxicity

2019 ◽  
Vol 25 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Reza Heidari ◽  
Mohammad Reza Arabnezhad ◽  
Mohammad Mehdi Ommati ◽  
Negar Azarpira ◽  
Elham Ghodsimanesh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Liver Tissue ◽  
Acute Liver Injury ◽  
Experimental Models ◽  
Clinical Value ◽  
Protective Properties ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity ◽  
And Oxidative Stress

Background: The xenobiotics-induced liver injury is a clinical complication. Hence, finding new hepatoprotective strategies has clinical value. Oxidative stress and its subsequent complications are major mechanisms involved in xenobiotics-induced hepatotoxicity. Boldine is one of the most potent antioxidant molecules widely investigated for its protective properties in different experimental models. In the current study, the hepatoprotective properties of boldine and its potential mechanisms of hepatoprotection have been investigated. Methods: Rats received thioacetamide (TAA; 200 mg/kg, i.p) as a model of acute liver injury. Boldine (5, 10, 1nd 20 mg/kg; 24 hours intervals; oral) was administered as the hepatoprotective agent. Results: Liver injury was evident in TAA-treated animals (48 hours after TAA exposure) as a severe increase in serum level of liver injury biomarkers and histopathological alterations. Moreover, markers of oxidative stress were increased in liver tissue of TAA-treated rats. Assessment of mitochondrial indices of functionality revealed a significant decrease in mitochondrial dehydrogenases activity, the collapse of mitochondrial membrane potential, mitochondrial swelling and depletion of ATP content. It was found that boldine supplementation mitigated liver tissue markers of oxidative stress and improved mitochondrial indices of functionality in TAA-treated animals. Conclusion: The hepatoprotective properties of boldine might primarily rely on antioxidant and mitochondria protecting effects of this alkaloid.

246 Effects of Feeding Thermally Processed Spray-dried Egg Whites on Growth Performance, Apparent Digestibility, and Oxidative Stress in Nursery Pigs

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 91-92
Author(s):  
Victoria C Wilson ◽  
Brian J Kerr
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Liver Tissue ◽  
Protein Carbonyls ◽  
Nursery Pigs ◽  
Thermally Processed ◽  
Markers Of Oxidative Stress ◽  
Dietary Treatments ◽  
And Oxidative Stress ◽  
Spray Dried

Abstract The objectives of this study were to determine if feeding thermally processed (TP, heated at 100°C for 120 h) spray-dried egg whites (SDEW) to nursery pigs would impact growth performance, apparent total tract digestibility (ATTD) of GE, N, and S, and oxidative stress. Thirty-two barrows, (initial BW 7.1 kg) were randomly assigned to dietary treatments with 1 pig per pen. In a preliminary study, thermally processing SDEW at 100°C for 120 h increased protein carbonyls (PC) from 6 µmol/g to 19.4 µmol/g (P ≤ 0.01). Diets included either 12% SDEW, 6% TP-SDEW plus 6% SDEW, or 12% TP-SDEW. The experiment lasted 24 d for collection of growth performance data, while plasma was collected on d 21 and liver tissue harvested on d 24 to analyze for markers of oxidative stress. Feces were collected on d 22 for measures of ATTD. Daily gain, daily feed intake, feed efficiency, and ATTD of GE were not found to be different among dietary treatments (P ≥ 0.57). In contrast, ATTD of N (P = 0.11) and S (P = 0.03) were found to increase with increasing protein oxidation in the diet. There was no change in the plasma or liver F2-isoprostanes and 8-hydroxy-2’-deoxyguanosine among dietary treatments (P ≥ 0.28). An increase in plasma PC (P = 0.02) was observed in pigs fed 12% TP-SDEW compared to pigs fed 12% SDEW and pigs fed 6% TP-SDEW. In contrast, a decrease in liver tissue PC (P = 0.04) was observed in pigs fed 6% TP-SDEW compared to pigs fed 12% SDEW and 12% TP-SDEW. These results indicate that feeding TP-SDEW does not affect growth performance, ATTD of GE, and oxidative stress as indicated by F2-isoprostanes or 8-hydroxy-2’-deoxyguanosine; but appeared to have variable effects on oxidative stress as measured by PC.

scholarly journals Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. S. Bruells ◽  
P. Duschner ◽  
G. Marx ◽  
G. Gayan-Ramirez ◽  
N. Frank ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Liver Injury ◽  
Liver Damage ◽  
Acute Liver Injury ◽  
Serum Levels ◽  
Acute Liver Damage ◽  
Markers Of Inflammation ◽  
Amino Phenol ◽  
And Oxidative Stress

AbstractN-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.

Cytoprotective potential of tiron and methyl palmitate against acetaminophen-induced acute liver injury

2016 ◽  
Vol 94 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Amal M. Shoeib ◽  
Eman Said ◽  
Elsayed M. Ammar
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Inflammatory Response ◽  
Biochemical Markers ◽  
Methyl Palmitate ◽  
Inflammatory Cytokine ◽  
Acute Liver Injury ◽  
Histopathological Examination ◽  
Hepatoprotective Effects ◽  
And Oxidative Stress

Acute liver injury is a debilitating disorder associated with loss of synthetic and detoxifying functions of the liver. This investigation was designed to assess cytoprotective efficacy of daily oral tiron (300 mg/kg) and daily oral methyl palmitate (300 mg/kg) against acetaminophen-induced acute liver injury. Rats were orally pretreated with either tiron or methyl palmitate at doses (300 mg/kg) for 7 days prior to oral acetaminophen (3 g/kg). Biochemical assay of markers of hepatotoxicity indices and oxidative stress was undertaken. Expression of inflammatory cytokine IL-6 was also evaluated. Histopathological examination of liver specimens was carried out as well. Both methyl palmitate and tiron significantly reversed the acetaminophen-induced elevation of biochemical markers (ALT, AST, and ALP) with restoration of SOD levels. Serum albumin levels and GSH liver contents increased, but in a nonsignificant manner. Moreover, methyl palmitate and tiron significantly decreased the level of serum LDH and serum IL-6 levels. Histopathology revealed that tiron markedly reduced the extent of acetaminophen-induced necrosis and methyl palmitate moderately decreased the necrosis in liver tissue. Methyl palmitate (300 mg/kg) and tiron (300 mg/kg) demonstrated promising hepatoprotective effects against acetaminophen-induced acute liver injury via modulation of inflammatory response and alleviation of the oxidative stress, allowing the preservation of hepatic functions.

Sign in / Sign up

Export Citation Format

Share Document