Dissolved methane during hypoxic events at the Boknis Eck Time Series Station (Eckernförde Bay, SW Baltic Sea)

Dissolved CH4 was measured in the water column at the Boknis Eck (BE) time series station in the Eckernförde Bay (SW Baltic Sea) on a monthly basis from June 2006 to November 2008. The water column at BE was always supersaturated with CH4 and, therefore, CH4 was released to the atmosphere throughout the sampling period: the mean CH4 surface (1 m) saturation at BE was 554±317%. A pulse of enhanced CH4 emissions occurs when the CH4 accumulation in the hypoxic bottom layer during summer is terminated in late summer/autumn. We did not detect a straightforward relationship between periods of enhanced CH4 in the bottom layer and hypoxic events at BE: the sedimentary release of CH4 seemed to be mainly triggered by sedimenting organic material from phytoplankton blooms. We conclude that future CH4 emissions from BE will be determined by the intensity of phytoplankton blooms, which in turn will be influenced by eutrophication. However, hypoxic events seem to have only a modulating effect on the enhancement of sedimentary methanogenesis and the subsequent release of CH4 to the water column

Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. In mice, lovastatin mitigated acute doxorubicin-induced heart and liver damage as indicated by reduced mRNA levels of the pro-fibrotic cytokine connective tissue growth factor (CTGF) and pro-inflammatory cytokines, respectively. Lovastatin also protected from doxorubicin-provoked subacute cardiac damage as shown by lowered mRNA levels of CTGF and atrial natriuretic peptide. Increase in the serum concentration of troponin I and cardiac fibrosis following doxorubicin treatment were also reduced by lovastatin. Whereas protecting the heart from harmful doxorubicin effects, lovastatin augmented its anticancer efficacy in a mouse xenograft model with human sarcoma cells. These data show that statins lower the incidence of cardiac tissue injury after anthracycline treatment in a Rac1-dependent manner, without impairing the therapeutic efficacy