Understanding the Environmental Impact of a Mine Dam Rupture in Brazil: Prospects for Remediation.

The rupture of the Fundão mine dam in Mariana municipality, Minas Gerais State, Brazil, spilled the tailings across the Doce River basin. These tailings, composed of residues discarded from the beneficiation of iron ore, are rich in SiO and AlO, as well as some ether amine compounds and NaOH. The aim of this study was to assess the distribution of these sediments, as well as their effect on the riparian zones reached, as compared with preserved sites. Sediment deposition in the river resulted in a morphological change from a meandering profile to a braided aspect. The nutrient and mineral content (P, K, Ca, Mg, Cu, Fe, Mn, Zn, and NO) and soil organic matter of the sediments were depleted, whereas NH, Na, and pH increased. A random presence of ether amines in the sediments was confirmed by quantitative and chromatographic analyses, with concentrations ranging from 0 to 57.8 mg kg; Na reached values as high as 150 mg kg. The impact of the dam tailings on biota was assessed by estimating total microbial biomass (phospholipid fatty acids), which were depleted in sediments relative to soils from preserved sites. Overall plant mortality, as well as a low resilience capacity, were also observed. Ether amines and Na present in the sediments had a strong toxic effect in the environment. Identification of these substances as the main impact factors will help guide future remediation efforts.

Nitric oxide donor FK409 and 8-bromoguanosine-cyclic monophosphate attenuate cardiac contractility assessed by Emax.

FK409 decomposes and releases nitric oxide (NO) spontaneously when it is dissolved in phosphate buffer solution at 37 degrees C. With the use of this NO donor, the effect of exogenous NO on cardiac contractility was examined by assessing Emax. alpha-chloralose-anaesthetized dogs were instrumented for measurements of left ventricular (LV) pressure and volume and coronary blood flow (CBF) in the left anterior descending artery (LAD). FK409, 8-bromoguanosine-cyclic-monophosphate (8-Br-cGMP) and papaverine were infused into the LAD, and Emax was determined by transient inferior vena cava occlusion when CBF was increased and reached its peak. Neither drug affected heart rate nor LV pressure just before the measurement of Emax. FK409 increased CBF and decreased Emax in a dose-dependent manner. 8-Br-cGMP also increased CBF and decreased Emax in a dose-dependent manner. Pretreating with propranolol did not affect the effects of FK4098-Br-cGMP on CBF and Emax. Papaverine increased mean CBF but did not affect Emax. In conclusion NO attenuates cardiac contractility in vivo, while increasing CBF. This effect seems to be mediated by cyclic-guanosine monophosphate, a second messenger of NO.