Soy is naturally high in isoflavones, a group of phytochemicals that show oestrogenic activity. Soy isoflavones can interact with the oestrogen receptor in mammals including humans, and this allows alteration of the hormonal milieu and an increase in the risk of cell proliferation that may initiate cancer. As well as these oestrogenic effects, soybeans may also interact with the thyroid gland, and the association between soybean consumption and goitre is well reported in the nutritional literature. In particular it has been shown that rats and human infants with borderline iodine intakes can develop goitre, that is reversible either through the removal of soy from the diet or through increasing iodine intake. Adolescent humans fed soy formula diets as infants show twice the prevalence of autoimmune disorders relating to thyroid function compared to those who were not exposed to soy as infants. Adults fed 30 grams of pickled soybeans per day developed goitre and elevated thyroid stimulating hormone levels within 1 month.
Thyroid peroxidase is a haem containing enzyme found in the cell membranes of thyroid producing cells. Thyroid peroxidase is required for the synthesis of thyroid hormone and because of this its activity is a useful marker to assess the effects of antithyroid compounds. Lactoperoxidase is a similar enzyme that can be substituted for thyroid peroxidase in models of thyroid activity because both enzymes have overlapping functions. Soy isoflavones have been shown to inhibit both thyroid peroxidase and lactoperoxidase, and analysis shows that daidzein and genistein are responsible for this effect. Both daidzein and genistein, in the absence of iodide, bind covalently to the active site of the enzyme. This binding prevents the enzyme binding its substrate, rendering the enzyme inactive. When adequate iodide in present both genistein and daidzein become substrates for the enzymes resulting in the production of mono-, di- and triiodoisoflavones, which are not be biochemically useful.
Addition of genistein to the diet of young rats has been shown to have endocrine disrupting effects. Administration of genistein in concentrations of 0, 5 100 and 500 parts per million were made to female rats 4 weeks before mating and continuing until weaning. The offspring then consumed the same diet as their mother before being sacrificed and examined at day 140 postpartum. The concentration of genistein in the rats at the 500 parts per million level resulted in tissue concentrations of genistein similar to humans fed soy formulas. The predominant metabolite of genistein in the rats were glucuronides, as has also been shown in humans. Genistin (the unconjugated form) showed preferential accumulation in the thyroid tissue of the rats. Analysis revealed that the genistin had caused inactivation of thyroid peroxidase in the rats with 80 % loss of thyroid peroxidase activity in the 500 parts per million rats. However the lower doses also showed evidence of inactivated thyroid peroxidase enzyme activity.
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