scholarly journals Calcium-deficient diet attenuates carbon tetrachloride-induced hepatotoxicity in mice through suppression of lipid peroxidation and inflammatory response

Heliyon ◽  
2016 ◽  
Vol 2 (6) ◽  
pp. e00126 ◽  
Author(s):  
Hiroki Yoshioka ◽  
Tsunemasa Nonogaki ◽  
Nobuyuki Fukuishi ◽  
Satomi Onosaka
2011 ◽  
Vol 205 ◽  
pp. S185
Author(s):  
L. Knockaert ◽  
C. Ribault ◽  
A. Fautrel ◽  
S. Lepage ◽  
J. Bégué ◽  
...  

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.


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