Vitamin E dietary supplementation protects against carbon tetrachloride—induced chronic liver damage and cirrhosis

✍ Scribed by Dr. Maurizio Parola; Gabriella Leonarduzzi; Fiorella Biasi; Emanuele Albano; Maria E. Biocca; Giuseppe Poli; Mario U. Dianzani

• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 933 KB
• Volume: 16
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840160426

✦ Synopsis

Previous studies have shown that a-tocopherol (vitamin E) pretreatment of experimental animals can protect against acute liver necrosis induced by carbon tetrachloride. In this study we investigated whether the increase of vitamin E liver content by dietary supplementation influences chronic liver damage and cirrhosis induced by carbon tetrachloride in the rat.

Our data indicate that vitamin E supplementation did not interfere with the growth rate of the animals and increased about threefold the liver's content of the vitamin. Vitamin E supplementation significantly reduced oxidative liver damage, but it was not effective in protecting against development of fatty liver and did not interfere with metabolic activation of carbon tetrachloride. Moreover, vitamin &fed animals showed incomplete but significant prevention of liver necrosis and cirrhosis induced by carbon tetrachloride. This has been shown by means of histological examination, analysis of serum parameters and biochemical evaluation of collagen content. These results show that an increased liver content of vitamin E can afford a significant degree of protection against carbon tetrachlorideinduced chronic liver damage and cirrhosis. (HEPATOLOGY 1992; 16.1014-102 1)

Liver necrosis has been considered the driving force in initiation and progression of cirrhosis, regardless of the cause of hepatocyte injury and death (1). It is well known that fibrosis occurs when parenchymal injury becomes chronic; the process itself is seen as the expression of altered regulation of the normal response of the organ to cell damage (i.e., regeneration) (2). This altered regulation occurs in relation to the development of inflammatory reactions and presumably affects the cytokinemediated interrelationships among different nonparen-