scholarly journals Protective Action of Antioxidants on Hepatic Damage Induced by Griseofulvin

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
M. del C. Martinez ◽  
S. G. Afonso ◽  
A. M. Buzaleh ◽  
A. Batlle

Erythropoietic protoporphyria (EPP) is a disease associated with ferrochelatase deficiency and characterized by the accumulation of protoporphyrin IX (PROTO IX) in erythrocytes, liver, and skin. In some cases, a severe hepatic failure and cholestasis were observed. Griseofulvin (Gris) develops an experimental EPP with hepatic manifestations in mice such as PROTO IX accumulation followed by cellular damage as wells as necrotic and inflammatory processes. The antioxidant defense system was also altered. The aim was to evaluate the possible protective effect of different antioxidant compounds: trolox (Tx), ascorbic acid (Asc), the combination Tx and Asc, melatonin (Mel), and the polyphenols: ellagic acid, quercetin, chlorogenic acid, caffeic acid, gallic acid, and ferulic acid on liver damage and oxidative stress markers in a mouse model of EPP. Coadministration of Gris with Tx, Asc, and its combination, or Mel mainly affected heme biosynthetic pathway, resulting in a decrease in ALA-S activity which was increased by Gris, while the tested polyphenols exerted a protective effect on oxidative stress, decreasing lipid peroxidation and the activity of some antioxidant enzymes. In conclusion, antioxidant compounds can only protect partially against the liver damage induced by Gris, reducing oxidative stress or acting on heme regulation.

2019 ◽  
Vol 24 (40) ◽  
pp. 4825-4837 ◽  
Author(s):  
Gustavo Alberto de la Riva ◽  
Francisco Javier López Mendoza ◽  
Guillermin Agüero-Chapin

Background: Oxygen is involved in a variety of physiological reactions in aerobic organisms, such as those produced in the electron transport chain, hydroxylation, and oxygenation. Reactive oxygen species (ROS) are naturally formed as byproducts from these previously reactions involving the O2 molecule; they are made up of superoxide anion (O2−), hydroxyl radical (HO−), hydrogen peroxide (H2O2), nitric oxide (NO), peroxyl (ROO−), and reactive aldehyde (ROCH). Under certain environmental stress conditions, ROS are accumulated causing cellular damage but also triggering the overexpression of several enzyme classes such as superoxide dismutases (SOD), catalases (CAT) and glutathione peroxidases (GPx), which represent an important intrinsic antioxidant defence line. Liver is a key organ in vertebrates including farm animals and human. The oxidative stress plays an important role in systemic malfunctions including hepatic, renal and immunological, disorders. Methods: This review presents a brief update about the relationship of oxidative stress with hepatic, renal and immunological malfunctions in stressed organisms. Cellular and exogenous hepatoprotective compounds share also the ability to scavenge ROS acting as antioxidants and in many cases as stimulators of immune response in stressed organisms. We present the effect of some hepatoprotectors on the hepatic, renal and immunological function in stressed mice by the jointed evaluation of biological and oxidative stress markers. Conclusion: Hepatoprotective effect of several exogenous compounds is very associated with their antioxidant capacity. This fact is relevant for keeping oxidant/antioxidant balance in the respective organs, but also for maintaining the physiological status of the whole organism.


2014 ◽  
Vol 40 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Khalid Mohammed Naji ◽  
Maher Ali Al-Maqtari ◽  
Adnan Ali Al-Asbahi ◽  
Qais Yusuf M. Abdullah ◽  
R. Nagesh Babu ◽  
...  

2018 ◽  
Vol 35 (2) ◽  
pp. 375-383
Author(s):  
S.A Hussein ◽  
O.M Abd el-hamid ◽  
O.S El-tawil ◽  
E.S Laz ◽  
W.M Taha

Author(s):  
Heba Abdulmohsin ◽  
Ahmed Abu Raghif ◽  
Mohammed Jabbar Manna

Objective: The aim of this study was to investigate antioxidant and hepatoprotective properties of Iraqi Echinops heterophyllus aqueous crude extract and its flavonoid fraction against methotrexate (MTX)-induced hepatotoxicity in rabbits.Methods: MTX-induced hepatotoxicity by administration of 20 mg/kg MTX intraperitoneally for 3 successive days was used as animal model, and animals were arrayed in four groups with eight animals in each group: Group 1 was the healthy control, Group 2 - the negative control receiving MTX only, Group 3 received MTX+crude extract of E. heterophyllus, and Group 4 administered MTX+flavonoid fraction of E. heterophyllus. The study duration was 10 days; at day 11, animals were sacrificed, and the blood samples were obtained for the measurement of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, total protein, and albumin as well as ELISA assay of the oxidative stress markers such as glutathione (GSH) and malondialdehyde (MDA). The liver was dissected and processed for histopathological investigation and scoring. Statistical analysis was performed to investigate the significance of each result.Results: The study results revealed severe liver damage due to MTX administration in the negative control (induced-non treated) group in comparison with healthy group, also there was significant hepatoprotective effect after administration of the crude extract of E. heterophyllus, and flavonoid fraction from E. heterophyllus shown after biochemical liver function tests and anti-oxidant properties demonstrated by the measurement of oxidative stress markers MDA and GSH. The crude extract of E. heterophyllus shown superior hepatoprotective and antioxidant effect. Histopathological scoring showed a remarkable decrease in the scores of the treatment groups in comparison with the high score in the MTX only treated group.Conclusions: MTX administered in a dose of 20 mg/kg for 3 successive days causes marked liver injury, while treatment with the crude extract and flavonoid fraction of E. heterophyllus significantly ameliorates MTX-induced liver damage, although the crude extract of E. heterophyllus seems to have the most hepatoprotective properties.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Ilaria Peluso ◽  
Maura Palmery

It has been suggested that some fruit-based drinks (FBD) may delay the onset of postprandial stress, which is involved in the pathogenesis of many diseases. The majority of the studies, which have investigated the effects of FBD on postprandial stress, involved a placebo that was a drink with the same content in sugars or carbohydrates of the FBD, but without the bioactive antioxidant compounds. These studies were aimed more at evaluating the effect of the antioxidants rather than the effect of the FBD as a whole. Only 4 studies compared the effect of FBD with water as control and did not support the hypothesis that FBD could inhibit postprandial dysmetabolism, as well as the studies that compared the effect of orange juice and cola. Overall, the results suggest a complex relationship between postprandial dysmetabolism, inflammation, and oxidative stress. Furthermore, the inflammatory and oxidative stress markers need further analytical validation and normal ranges should be established in order to reach a firm conclusion. Finally, caution should be taken in the interpretation of the effect of FBD in postprandial studies and the reviewed results suggest that dietary recommendations should aim to limit rather than increase sugar-sweetened beverages consumption.


2021 ◽  
Author(s):  
Wen Nie ◽  
Ye-ye Du ◽  
Fei-ran Xu ◽  
Kai Zhou ◽  
Zhao-ming Wang ◽  
...  

Lys-Arg-Gln-Lys-Tyr-Asp bioactive peptide in JHP prevent ALD by regulating gut microbiota, upregulating the expression of the NRF2/HO-1 antioxidant defense system and reducing oxidative stress injury in liver cells.


2015 ◽  
Vol 37 (6) ◽  
pp. 2160-2170 ◽  
Author(s):  
Preeti Kanikarla-Marie ◽  
Sushil K. Jain

Background/Aims: Type 1 diabetic (T1D) patients have a higher incidence of liver disease. T1D patients frequently experience elevated plasma ketone levels along with hyperglycemia. However, no study has examined whether hyperketonemia per se has any role in excess liver damage in T1D. This study investigates the hypothesis that hyperketonemia can induce oxidative stress and cellular dysfunction. Methods: STZ treated diabetic rats, FL83B hepatocytes, and GCLC knocked down (GSH deficient) hepatocytes were used. Results: The blood levels of ALT and AST, biomarkers of liver damage, and ketones were elevated in T1D rats. An increase in NOX4 and ROS along with a reduction in GSH and GCLC levels was observed in T1D rat livers in comparison to those seen in non-diabetic control or type 2 diabetic rats. MCP-1 and ICAM-1 were also elevated in T1D rat livers and ketone treated hepatocytes. Macrophage markers CCR2 and CD11A that interact with MCP-1, and ICAM-1 respectively, were also elevated in the T1D liver, indicating macrophage infiltration. Additionally, activated macrophages increased hepatocyte damage with ketone treatment, which was similar to that seen in GCLC knockdown hepatocytes without ketones. Conclusion: Hyperketonemia per se can induce macrophage mediated damage to hepatocytes and the liver, caused by GSH depletion and oxidative stress up regulation in T1D.


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