Zusammenfassung
Jod und seine Stoffwechselprodukte spielen in der Brustdrüse
offenbar eine ebenso entscheidende Rolle in der Wachstumsregulation und der
Entstehung von Neoplasien wie in der Schilddrüse. Jodmangel bei Ratten
erzeugt nicht nur Strumen, sondern auch Zellatypien, Dysplasien und
Hyperplasien der Brustdrüsen. In Tierversuchen konnte gezeigt werden, dass
Jod bzw. Seetang, nicht aber Jodid in der Nahrung die Entstehung von chemisch
erzeugten Mammakarzinomen signifikant verzögert. Die chronische Zufuhr von
Jod kann die Inzidenz von chemisch induzierten Mammakarzinomen bei Ratten um
70 % reduzieren. Bereits bestehende Tumore werden unter einer hohen
Jodzufuhr auch kleiner, ohne die Schilddrüsenfunktion zu
beeinträchtigen. Die Tumore haben eine höhere Jodkonzentration als
das gesunde Gewebe, und dies kann durch Progesteron noch gesteigert werden.
Bei den menschlichen Mammakarzinomen wird in etwa zwei Drittel der
Fälle NIS exprimiert und radioaktives Jod aufgenommen. Interessanterweise
wird diese Jodaufnahme im Gegensatz zur Schilddrüse durch Perchlorat nicht
blockiert. In Experimenten mit humanen Brustkrebs-Zellkulturen (MCF7) konnte
eindeutig belegt werden, dass die Proliferation durch Jod, nicht aber Jodid
gehemmt wird. Auch wird durch Jod eine Apoptose in malignen Mammakarzinomzellen
induziert. Es entstehen Jodlipide, insbesondere δ-Jodlacton aus
Arachidonsäure (6-iodod-5-hydroxy-eicosapentaensäure), das für
diesen hemmenden Effekt verantwortlich zu sein scheint. Dieses
δ-Jodlacton wurde bereits vor einiger Zeit in der Schilddrüse als
das wesentliche Intermediärprodukt charakterisiert, das nicht nur die
Proliferation von Schilddrüsenzellen hemmen, sondern auch deren Apoptose
induzieren kann. Es gibt somit zahlreiche Untersuchungen, die bereits gezeigt
haben, dass eine ausreichend hohe Jodzufuhr nicht nur die hyperplastischen
Veränderungen der Schilddrüse, sondern möglicherweise auch der
Mamma verhindern kann und möglicherweise auch als adjuvante Therapie beim
Mammakarzinom eingesetzt werden könnte.
Summary
Iodine is essential in maintaining not only the normal thyroid
function and prevention of hyperplasia as well as neoplasia but seems also to
be essential for the breast to prevent neoplasias. Iodine deficiency renders
the rat thyroid and breast susceptibility to atypia, dyplasia and hyperplasia.
In animal trials it could be shown, that iodine or extracts of seaweed but not
iodide prevent chemically induced breast cancer. Iodine in conjunction with
progesterone and seaweed diet regresses chemically induced breast cancer in
animals. The tumours contain more iodine indicating more iodine trapping than
normal tissue. In addition increased apoptosis had been identified within the
tumours. Iodine treatment of patients with benign breast disease induces a
significant bilateral reduction in breast size and causes a remission of
disease symptoms.
Around two-third of human breast carcinomas express the
sodium-iodine symporter (NIS), which is identical to the thyroid specific NIS
and therefore trap radioactive iodine, but in the breast tumours iodine uptake
is not blocked by perchlorate like in the thyroid gland. In human breast cancer
cell lines it could be shown that iodine, but not iodide inhibit growth and
induces apoptosis in a caspase-independent pathway. It recently could be shown
that in this cell lines δ-iodolactone, an iodinated product of the cell
membrane arachidonic acid (6-iodo-5 hydroxy-eicosapentaenic acid) is generated.
This product has already been shown to regulate proliferation of thyroid cells
and also induces apoptosis. Up to now there are several in vitro as well as in
vivo studies that clearly demonstrate that iodine is important for the
prevention of benign as well as malignant breast disease and probably might be
an efficient adjuvant treatment in breast cancer.
Schlüsselwörter
Jod - Jodid - δ-Jodlacton - Brusterkrankungen - Brustkrebs
Keywords
Iodine - Iodide - δ-iodolactone - Breast disease - Breast cancer
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Korrespondenzadresse
Prof. Dr. med. Roland Gärtner
Medizinische Klinik Innenstadt
der Universität
München
Ziemssenstr. 1
80336 München
Email: roland.gaertner@med.uni-muenchen.de