Silymarin Protection Against Hepatic Lipid Peroxidation Induced by Acute Ethanol Intoxication in the Rat
 
   

Silymarin Protection Against Hepatic
Lipid Peroxidation Induced by Acute
Ethanol Intoxication in the Rat

This section is compiled by Frank M. Painter, D.C.
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   Frankp@chiro.org
 
   

FROM:   Biochem Pharmacol 1985 (Jun 15);   34 (12):   2209–2212

Valenzuela A, Lagos C, Schmidt K, Videla LA


The administration of silymarin to fed rats resulted in no changes in the basal lipid peroxidative rate of the liver. However, when the flavonoid was given prior to acute ethanol treatment, it was able to completely suppress the increases in hepatic MDA formation and in spontaneous chemiluminescence observed when ethanol was given alone. Possible mechanisms which may be responsible for the inhibition of ethanol-induced liver lipid peroxidation by silymarin pretreatment include the following. (i) Silymarin by itself could act as a free radical scavenger intercepting those radicals involved in ethanol metabolism by microsomal enzymes. Thus, by trapping oxygen-related free radicals, silymarin could hinder their interaction with polyunsaturated fatty acids and would abolish the enhancement of lipid peroxidative processes leading to MDA formation and light emision. In this respect, silymarin would share with (+)-cyanidanol-3, an antioxidant mechanism of action acting as free radical scavengers. (ii) Silymarin pretreatment exhibited a novel effect on the glutathione status of the liver cell, not observed in experiments using (+)-cyanidanol-3. Silymarin significantly increased the hepatic content of both GSH and GSSG, thus enhancing by 32% the content of total GSH equivalents (GSH + 2GSSG) of the liver, when compared to control rats given CMC. It is important to point out that this effect of silymarin administration did not alter the glutathione redox state of the liver, as the GSH/GSSG ratio was not modified by the treatment. Silymarin-induced enhancement in total GSH equivalents expressed per g of liver was also observed when values are referred to body weight (Control CMC: 267.0 ± 25.3 (6) µmoles/kg body weight; Silymarin: 392.0 ± 14.1 (6); 46% increase; P < 0.005) or to hepatic protein content (Control CMC: 47.3 ± 4.0 (6) nmoles/mg protein; Silymarin: 60.1 ± 3.2 (6); 27% increase; P < 0.005) due to the lack of effect of the flavonoid on these reference parameters. These results suggest that a higher content of glutathione in the liver, in conditions in which its redox state is kept constant, would afford the tissue a better protection against an oxidative stress, thus contributing to the abolishment of ethanol-induced lipid peroxidation. This is supported by the lack of changes in the GSH/GSSG ratio following ethanol administration in silymarin-pretreated rats compared to the drastic decrease (68%) found when ethanol was given alone. The mechanism of silymarin-induced enhancement of hepatic glutathione content is currently under study in our laboratory.


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