Hg Pollution Indices along the Reis Magos River Basin-Brazil: A Precursory Study.

Mercury is a metal present in the Earth's crust, but due to human contribution, its concentration can increase, causing environmental impacts to aquatic ecosystems, among others. The Reis Magos River Hydrographic Basin represents economic and socio-environmental importance for the state of Espírito Santo, Brazil. However, there are not many publications regarding the quality of water and sediments, so no data is reported concerning the total concentration of Hg. Thus, the present work aimed to evaluate the distribution of total Hg in water and sediments along this hydrographic basin. For a better inference, physicochemical parameters of the water were determined (temperature, pH, electrical conductivity, oxidation-reduction potential (ORP), turbidity, dissolved oxygen (DO), total dissolved solids (TDS), and salinity), and in the sediments, the contents of matter organic matter, pH, carbonates and granulometry. Mercury determination was performed by Thermodecomposition and Amalgamation Atomic Absorption Spectrometry (TDA AAS) with a DMA-80 spectrometer. The Hg determined in the water was lower than the limit of quantification, 0.14 µg∙L-1, which is lower than the maximum limits recommended by world reference environmental agencies. In the sediment samples, the Hg found were below 170 µg∙kg-1, values below which there is less possibility of an adverse effect on the biota. However, when the degree of anthropic contribution was evaluated using the Geoaccumulation index (IGeo), the contamination factor (CF), and the ecological risk potential index (EF), there was evidence of moderate pollution. Thus, this highlighted the need for monitoring the region since climatic variations and physical-chemical parameters influence the redistribution of Hg between the water/sediment interface.

Low-level lead exposure changes endothelial modulation in rat resistance pulmonary arteries.

Lead exposure induces hypertension and endothelial dysfunction. However, the effects on the pulmonary vasculature have not been explored. In this study, rats exposed to lead acetate for seven days (4µg/100g on the 1st day and 0.05µg/100g/day i.m. subsequently) had lead blood level of 3.9±0.7µg/dL and increased right ventricular pressures. There was an increased Pb deposition and superoxide anions production in the pulmonary arteries, associated with reduced vasoconstriction but unchanged endothelium-dependent vasodilatation to acetylcholine (ACh). In both groups, inhibition of the nitric oxide (NO) synthase with L-NAME blocked the response to ACh, while indomethacin (cycloxygenase inhibitor) had no effect. Incubation with nonspecific potassium channel blocker (tetraethylammonium) reduced the ACh-induced vasodilatation only in the Pb group. Apamin (SKCa channel blocker) and 4-aminopyridine (Kv channel blocker), but not iberiotoxin (BKCa channel blocker), also inhibited this response in the Pb group. The vasodilatation to exogenous NO was reduced by Pb, while relaxation to the cGMP analogue was similar between groups. Concordantly, the protein level of soluble guanylate cyclase (sGC) was reduced. In conclusion, short-term and low-level exposure to Pb changes pulmonary haemodynamic and increases oxidative stress. The pulmonary vasculature exhibited increased hyperpolarization by the Kv and SKCa channels, probably as a compensatory mechanism to the decreased responsiveness to NO.