scholarly journals EFFECT OF DIFFERENT VEHICLES ON HEPATO- PROTECTIVE EFFICIENCY OF DESFERRIOXAMNE IN RADIATED CARBON TETRACHLORIDE TREATED MICE

2003 ◽  
Vol 71 (1) ◽  
pp. 19-34
Author(s):  
lbrahim El-Bagory ◽  
Mahmoud Mansour

The effect of desferrioxamine (DFO) in different vehicle ( Aqueous and oily) against hepatotoxicity induced by carbon tetrachloride (CC14) in irradiated mice and irradiated carbon tetrachloride (IR-CCI4) in normal mice was investigated. A single dose of CC14 and IR-CCI4 (20 @/kg, i.p.) in irradiated mice (IR-mice) and normal mice induced hepatotoxicrty, manifested biochemically by significant elevation of serum enzyme activities, such as alanine trarsaminase (ALT, EC:2.6.1.2 ) and aspartate transaminase (AST, EC:2.6.1.1). Hepatotoxiaty was further evidenced by significant decrease of total sulfttydryl (-SH) content, and catalase (EC: 1.1 1.1.6) activrty in hepatic tissues and significant increase in hepatic lipid peroxidation measured as malondialdhyde (MDA). Pretreatment of normal mice and IR-mice with DFO (200 mg/kg i.p dissolved either in water or arachis oil vehicle) 1 h before CC14 or IR-CC14 injection ameliorated the hepatotoxicrty as evidenced by a significant reduction in the elevated levels of serum enzymes as well as a significant decrease in the hepatic MDA content and a significant increase in the total sulfhydryl content 24 h after CC14 or IR-CCI4 administration.. These results indicated that both of oily and watery DFO can effectively ameliorated the hepatotoxicity induced by CC14 in IR-mice or IR-CC14 in normal mice. Although, the efficiency of the hepatoprotective effect of DFO in oily vehicle was higher than that DFO in aqueous vehicle. The hepatoprotective effect of DFO possibly through inhibition of the production of oxygen free radicals that cause lipid peroxidation.

1990 ◽  
Vol 11 ◽  
pp. S14 ◽  
Author(s):  
J. Camps ◽  
T. Bargálló ◽  
S. Alié ◽  
A. Giménez ◽  
J. Caballerla ◽  
...  

Author(s):  
Pablo Muriel ◽  
Nicolas Alba ◽  
Victor M Pérez-Álvarez ◽  
Mineko Shibayama ◽  
Victor K Tsutsumi

Author(s):  
L. Yusuf ◽  
M.K. Oladunmoye ◽  
A.O. Ogundare

Hepatoprotective assay was carried out on laboratory animals in which paracetamol (oral dose,2 g/kg /body weight) was used to induce hepatotoxicity. The animals were orogastrically fed with the Viscum album (growing on cocoa and cola host trees) methanolic leave extracts. The activities of serum enzyme biomarkers showed no significant difference (P< 0.05) for V. album growing on cocoa (1000-5000mg/kg) but there were corresponding significant increase in the serum enzymes (P< 0.05) for V. album growing on cola at 4000 and 5000 mg/kg doses. Similarly, the photomicrograms of the animals’ vital organs (liver, stomach, small intestine and kidneys) studied revealed that V.album extract growing on cocoa was more hepatoprotective efficacious than that growing on cola tree on all the biochemical parameters that were screened for when compared with sylimarin (a standard heptoprotective drug).


1992 ◽  
Vol 83 (6) ◽  
pp. 695-700 ◽  
Author(s):  
Jordi Camps ◽  
Teresa Bargallo ◽  
America Gimenez ◽  
Silvia Alie ◽  
Joan Caballeria ◽  
...  

1. Lipid peroxidation and hepatic fibrogenesis were investigated in 25 carbon tetrachloride-treated rats and in 25 control animals. Rats were further divided into two groups to receive either a standard diet or one supplemented with zinc. From each group, animals were killed at weeks 3 and 18 of the experiment for histological and biochemical assessments which included hepatic lipid peroxide and collagen concentrations and plasma zinc concentration as well as the hepatic activities of proline hydroxylase and collagenase. 2. Results indicated that oral zinc supplementation was associated with a decrease in lipid peroxidation (mean 51%; P<0.05), collagen deposition (mean 32%; P< 0.001) and proline hydroxylase activity (mean 30%; P<0.05) at week 18, together with an increase in collagenase activity (mean 208%; P<0.01) at week 3, in carbon tetrachloride-treated rats. 3. There was a significant direct correlation between lipid peroxidation and proline hydroxylase activity in carbon tetrachloride-treated rats (r = 0.52; P<0.01) and also a significant inverse correlation between lipid peroxidation and plasma zinc concentration in these animals (r = −0.62; P<0.001). 4. These findings are consistent with the hypothesis that hepatic lipid peroxidation plays an important role in the aetiology of hepatic fibrogenesis and that zinc mitigates the process.


2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.


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