摘要：The induction and subsequent intracellular distribution of the 72-kDa heat shock (stress) protein (Hsp72) by exposure of cultured human alveolar (L-132) cells to dimethylarsinic acid (DMAA), a main metabolite of inorganic arsenics in mammals, were examined. A significant induction of Hsp72 in the cells was observed by exposure to 10 mM DMAA for 6h. The induction was similar to the case by arsenite for 6h or by heat treatment at 42°C for 3h. However, the nuclear distribution of Hsp72 differed greatly between DMAA and 42°C treatment or arsenite exposure, i.e., Hsp72 induced by exposure to DMAA accumulated not only in the nucleoli but also in the nucleoplasm, whereas that by 42°C or arsenite exposure did not accumulate in the nucleoplasm. Furthermore, the Hsp72 accumulated in the nucleus by DMAA exposure hardly diffused with the addition of ATP, suggesting that the DMAA-induced Hsp72 strongly binds to some macromolecules in the nucleus. The fact that Hsp72 induced by DMAA exposure accumulated in the nucleus of the cells may reflect a protective response toward the nucleus-specific damaging action of dimethylarsenics.
