Effect of dietary kelp on lipid peroxidation and glutathione peroxidase activity in livers of rats given breast carcinogen DMBA

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Abstract
In our previous study of female rats, a diet containing 2% of powdered fronds of Laminaria religiosa (kelp) had a remarkable inhibitory effect on mammary tumorigenesis induced by orally given 7,12‐dimethylbenz[a]anthracene (DMBA). In this study, the effect of the dietary kelp on lipid peroxidation and glutathione peroxidase (GSH‐Px) activity in the liver was studied in the same experimental system. Two separate short‐ and long‐term experiments were carried out on rats fed a diet with 2% kelp. DMBA (20 mg/kg body wt) was given to each animal 7 days after feeding began in short‐term experiment and 27 days later in long‐term experiment. Livers of all rats were obtained for quantitative determination and for histopathologic observation. Lipoperoxide in livers of the kelp‐fed rats was of normal value, almost the same as that of untreated control rats; however, lipoperoxide in livers of control rats was significantly higher than in the other two groups in both experiments. A marked fatty change in livers of control rats was demonstrated in hepatic cells in peripheral zones of lobules in long‐term experiment but not in short‐term experiment. In long‐term experiment, the amounts of GSH‐Px and selenium in livers of kelp‐fed rats were slightly less than those in untreated control rats but more than those in control rats. There was a more‐intense positive reaction in the hepatic cells in the peripheral zones of the lobules in the kelp‐fed and untreated rats and a less‐intense positive reaction in control rats. In short‐term experiment, contents of GSH‐Px and selenium were nearly proportional to determined concentration of lipoperoxide, suggesting that induction of the synthesis of this enzyme by excessive lipoperoxide took place to quench peroxide itself. The most‐intense positive reaction around fat droplets in the hepatic cells was in peripheral zones in control rats. Thus, concentrations of lipoperoxide, GSH‐Px, and selenium in livers of kelp‐fed rats showed almost same values as in untreated control rats in both experiments. Results may be interpreted as the minimization of the toxicity of orally given DMBA, by which excessive lipoperoxide is produced in liver, by dietary kelp. Mechanisms of dietary kelp include inhibition of DMBA absorption through intestinal tract by kelp as dietary fiber and partly antioxidation against free oxygen radicals by β‐carotene in kelp.
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