Protective effects of vitamin E on carbon tetrachloride-induced liver damage in rats

✍ Scribed by Mustafa Naziroğlu; Mehmet Çay; Bilal Üstündağ; Mesut Aksakal; Hayrettin Yekeler

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 407 KB
• Volume: 17
• Category: Article
• ISSN: 0263-6484
• DOI: 10.1002/(sici)1099-0844(199912)17:4<253::aid-cbf837>3.0.co;2-r

✦ Synopsis

In this study we investigated whether the increase of hepatic vitamin E content by intraperitoneal administration, in¯uences chronic liver damage induced by carbon tetrachloride (CCl 4 ) in rats. Thirty adult male Wistar rats were divided into three groups. The ®rst group was used as a control and the rats in the second group were administered CCl 4 in olive oil subcutaneously. Rats in the third group were administered intraperitoneally vitamin E (dl-a-tocopherol acetate, 100 mg kg À1 ). This administration was performed three times per week for ®ve weeks. Liver samples were used for the determination of vitamin E levels, glutathione peroxidase (GSHPx) activities and histological examination.

Serum levels of alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, gamma-glutamyltranspeptidase, total and conjugated bilirubin were signi®cantly ( p 5 0 . 05, p 5 0 . 01, p 5 0 . 001) higher in animals treated with CCl 4 than in the controls and had returned to normal values by the administration of vitamin E CCl 4 . Liver vitamin E levels were signi®cantly ( p 5 0 . 05) lower in the CCl 4 group than in the control group. However, the liver vitamin E content was signi®cantly ( p 5 0 . 01, p 5 0 . 001) increased in the vitamin E CCl 4 injected group. On the other hand, liver GSHPx activity was not statistically dierent among the groups. On histological examination, vitamin E administered animals showed incomplete, but signi®cant, prevention of liver necrosis and cirrhosis induced by CCl 4 . these data indicate that intraperitoneally administered vitamin E has protective eects against CCl 4 -induced chronic liver damage and cirrhosis as evidenced by biochemical data and conventional histological examination.