One of the new challenges facing humanity is to reach increasingly further distant space targets. It is therefore of upmost importance to understand the behavior of microorganisms that will unavoidably reach the space environment together with the human body and equipment. Indeed, microorganisms could activate their stress defense mechanisms, modifying properties related to human pathogenesis. The host-microbe interactions, in fact, could be substantially affected under spaceflight conditions and the study of microorganisms' growth and activity is necessary for predicting these behaviors and assessing precautionary measures during spaceflight. This review gives an overview of the effects of microgravity and space radiation on microorganisms both in real and simulated conditions.

The present study aimed to evaluate the impact of polycyclic aromatic hydrocarbons (PAHs) produced by multiple emission sources on prokaryotic communities in sediments chronically affected by anthropogenic pressures. In this context, surface sediments were investigated in three Mediterranean touristic ports over three sampling periods and in different port sectors. The levels of 16 priority PAHs varied over three orders of magnitude (25-49,000 ng g −1) covering the range of concentrations previously reported for Mediterranean harbors. Pyrogenic processes were found to be the dominant emission source of PAHs, with considerable differences among ports. The prokaryotic communities were identified by using the terminal restriction fragment length polymorphism, targeting the 16S rRNA gene for Bacteria and Archaea as well as the dsrAB gene for sulphate-reducing bacteria (SRB). The structure of the three benthic prokaryotic communities varied consistently among the ports. The structure of Bacteria and Archaea exhibited strong spatiotemporal variations that did not allow us to specifically link the observed differences in community structures with PAH sources. On the contrary, our study provided, for the first time, evidence that the PAH emission sources play a role in structuring benthic communities of SRB. Our findings indicate that the SRB community can be used as a valuable candidate biotic descriptor for bioremediation monitoring in heavily impacted port sediments.

Doxorubicin (Doxo) is a widely used anticancer drug given for the treatment of leukemias, lymphomas, and solid tumors. Despite its potent antitumor effects, the cardiotoxicity of this drug limits its clinical use. The biochemical mechanisms of Doxo-induced cardiotoxicity remain unclear. Doxo has been shown to induce apoptosis in cardiomyocytes that seems to be responsible, at least in part, for Doxo cardiotoxicity. In this study, we investigated tumor necrosis factor-alpha (TNF-alpha) receptor-mediated signaling to better understand the causes of Doxo-induced cardiotoxicity. Here, we report that Doxo is a potent inducer of apoptosis in both H9c2 cardiomyocytes and U2OS osteosarcoma tumor cells, with significant differences in terms of kinetics and caspase activation between the two cell lines. Interestingly, Doxo-induced apoptosis is accompanied by relevant changes in TNF-alpha receptor levels in H9c2 cardiomyocytes but not in U2OS cells. Moreover, treatment with exogenous TNF-alpha strongly potentiates the apoptotic effect of Doxo in H9c2 cardiomyocytes but not in U2OS cells. Our findings show that the function of TNF receptors I and II is affected by Doxo to ultimately modulate apoptosis and cell survival in H9c2 cardiomyocytes, reinforcing the recent evidence of the relevant role of TNF-alpha receptor-mediated signaling in cardiotoxicity induced by anthracyclines.

In order to elucidate how phosphate regulates cellular functions, we investigated the effects of inorganic phosphate (Pi) on adenylate cyclase (AC)/cyclic AMP (cAMP) axis. Here we describe that Pi treatment of human osteosarcoma U2OS cells results in a decrease of both intracellular cAMP levels and AC activity, and in a cell growth inhibition. The phosphate-triggered effects observed in U2OS cells are not a widespread phenomenon regarding all cell lines, since other cell lines screened respond differently to parallel Pi treatments. In U2OS cell line, the AC activity/cAMP downregulation is accompanied by significant variations in the levels of some membrane proteins belonging to the AC system. Remarkably, the above effects are blunted by pharmacological inhibition of sodium-dependent phosphate transport. Moreover, 8-Br-cAMP and other cAMP-elevating agents, such as IBMX and forskolin, interestingly, prevent the cell growth inhibition in response to phosphate. Our results enforce the increasing evidences of phosphate as a signaling molecule, identifying in U2OS cell line the AC/cAMP axis, as a novel-signaling pathway modulated by phosphate to ultimately affect cell growth.