Abstrakt

Działanie wielu czynników egzogennych, a także zaburzone procesy metaboliczne komórek przyczyniają się do nasilonego wytwarzania oksydantów, a to zaburza równowagę redoks, wywołując zmiany metaboliczne, w tym śmierci lub transformacji nowotworowej komórek. Jednak każda komórka zawiera antyoksydanty, które mają zapobiegać tego typu sytuacjom. Jednym z układów antyoksydacyjnych, funkcjonujących w komórkach, jest układ zależny od tioredoksyny, w skład którego wchodzą: tioredoksyna (Trx), reduktaza tioredoksyny (TrxR) oraz peroksydaza tioredoksyny (TPx), które mogą redukować utlenione składniki komórek kosztem fosforanu dinukleotydu nikotynoamidoadeninowego (NADPH). Działanie takie wynika z budowy przestrzennej Trx oraz TrxR, która umożliwia wytworzenie wewnątrzcząsteczkowego mostka disulfidowego w obrębie cząsteczki tioredoksyny oraz dwóch międzycząsteczkowych mostków selenosulfidowych w obrębie dimeru reduktazy tioredoksyny. Inną, równie istotną funkcją układu zależnego od tioredoksyny jest regulowanie ekspresji wielu białek za pośrednictwem takich czynników jak czynnik transkrypcyjnego NF-κB oraz kinaza regulująca apoptozę (ASK-1), które uruchamiają kaskady przemian metabolicznych prowadzących ostatecznie do proliferacji lub apoptozy komórek. Wzrost ekspresji/aktywności składników systemu zależnego od Trx obserwuje się w rozwoju wielu nowotworów. Dlatego też poszukiwanie selektywnych inhibitorów tioredoksyny lub reduktazy tioredoksyny jest obecnie jednym z głównych kierunków badań w farmakoterapii nowotworów. Wykazano, że wiele naturalnie występujących związków polifenolowych pochodzenia naturalnego o działaniu antyoksydacyjnym (np. kwercetyna czy kurkumina) powoduje inaktywację układu Trx-TrxR. Jednocześnie wiele syntetycznych związków, w tym związki kompleksowe, które stosowane są w terapii przeciwnowotworowej (np. cisplatyna, auranofina, moteksafina gadolinu), również hamują działanie układu zależnego od Trx.

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