Cellular changes in boric acid-treated DU-145 prostate cancer cells

Epidemiological, animal, and cell culture studies have identified boron as a chemopreventative agent in prostate cancer. The present objective was to identify boron-induced changes in the DU-145 human prostate cancer cell line. We show that prolonged exposure to pharmacologically-relevant levels of boric acid, the naturally occurring form of boron circulating in human plasma, induces the following morphological changes in cells: increases in granularity and intracellular vesicle content, enhanced cell spreading and decreased cell volume. Documented increases in β-galactosidase activity suggest that boric acid induces conversion to a senescent-like cellular phenotype. Boric acid also causes a dose-dependent reduction in cyclins A–E, as well as MAPK proteins, suggesting their contribution to proliferative inhibition. Furthermore, treated cells display reduced adhesion, migration and invasion potential, along with F-actin changes indicative of reduced metastatic potential. Finally, the observation of media acidosis in treated cells correlated with an accumulation of lysosome-associated membrane protein type 2 (LAMP-2)-negative acidic compartments. The challenge of future studies will be to identify the underlying mechanism responsible for the observed cellular responses to this natural blood constituent

Cardiac sympathetic innervation imaging with myocardial MIBG scintigraphy [Studio dell'innervazione cardiaca mediante scintigrafia miocardica con MIBG]

Metaiodobenzylguanidine (MIBG) was developed initially as a tracer for oncological imaging; when labeled with 123 I or 131 I, it may detect APUDomas, such as pheochromocytomas and paragangliomas. In the last years, MIBG has found an important role also in neurology and cardiology, as cardiac innervation tracer. Actually, MIBG cardiac imaging is a universally accepted method to estimate cardiac sympathetic innervations. This review covers the role of MIBG cardiac imaging in Parkinson disease and parkinsonisms, from the pathophysiological premises for cardiac denervation to new emerging dat