DISTRIBUTION AND ABUNDANCE OF HEAVY METALS IN SEDIMENTS FROM VITÓRIA ISLAND ESTUARINESYSTEM. Heavy-metal concentration in sediment is an important parameter for identifying pollution sources and assessing pollution levels in aquatic ecosystems. In this context, the present study aimed at determining concentrations of heavy metals in sediments from the Vitória estuarine system, Brazil. Twenty nine stations were surveyed to assess the spatial distribution of heavy metals. The metals for silt-clay fractions (<63 µm) were analyzed through atomic absorption spectrometry. A discriminant analysis segregated the stations in four groups representing four areas within the estuarine system. The Espírito Santo Bay showed the lowest metal concentrations, while the Vitória harbor canal showed the highest. We concluded that concentrations of heavy metals reflect natural conditions and the contribution of human activities from sewage and industrial effluents. It was not possible to directly associate metal concentrations to specific pollution sources.Keywords: heavy metals; estuarine sediments; sewage. INTRODUÇÃOUma das grandes preocupações ecológicas atuais refere-se ao impacto ambiental causado pela liberação antrópica de metais pesados nos diversos ambientes naturais e, de maior importância, naqueles de maior interação com populações humanas. Tanto águas, materiais particulados, sedimentos como organismos aquáticos têm sido utilizados nesta avaliação, sendo que os três últimos compartimentos bióticos são preferíveis devido às facilidades de coleta, estocagem e tratamento das amostras (minimização de contaminação ou perdas), e às maiores concentrações encontradas, dispensando tarefas de pré-concentração e facilitando os procedimentos de análise 1,2 . Os sedimentos têm sido considerados como um compartimento de acumulação de espécies poluentes a partir da coluna d'água, devido às altas capacidades de sorção e acumulação associadas 3,4 , onde as concentrações tornam-se várias ordens de grandeza maiores do que nas águas correspondentes, possibilitando o uso dos mesmos como um bom indicador de poluição ambiental, tanto atual como remota (p.ex. através da estratificação 5 ), possibilitando ainda o conhecimento das principais fontes de poluição dentro de um determinado sistema aquático. Contudo, diversos processos bióticos e abióticos podem remobilizar tais espécies, constituindo-se em fontes de poluição secundárias 6,7 , afetando a qualidade da água e originando bioacumulação e trocas de transferência na cadeia trófica 1,8 . Em conseqüência, a contaminação de sedimentos é um importante problema ambiental em todo mundo.Muitos trabalhos têm sido publicados a respeito de metais pesados acumulados em sedimentos de regiões tropicais, principalmente em regiões costeiras fortemente industrializadas, como no estado do Rio de Janeiro, São Paulo e Bahia 4-6,9-13 . É interessante destacar o trabalho de Carvalho e Lacerda 4 na Baía de Guanabara onde, após análise química de diversos organismos marinhos bentônicos, não se observaram altas conc...

Chronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 µg/100 g, subsequent dose 0.05 µg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 µg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM–100 µM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM–300 µM) or sodium nitroprusside (0.01 nM–0.3 µM). Endothelium removal, N G-nitro-L-arginine methyl ester (100 µM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 µM) increased but losartan (10 µM) and enalapril (10 µM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na+/K+-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na+/K+-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na+/K+-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBP.

BackgroundChronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension.Methodology/Principal FindingsWistar rats were treated with lead acetate (i.v. bolus dose of 320 µg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na+,K+-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 µg/dL, which is below the reference blood concentration (60 µg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na+,K+-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na+,K+-ATPase, AT1 and AT2. Pre-treatment with an AT1 receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect.ConclusionAcute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular disease.

A procedure for the determination of As in diesel, gasoline and naphtha at microg L(-1) levels by GFAAS is proposed. Sample stabilization was achieved by the formation of three component solutions prepared by mixing appropriate volumes of the samples propan-1-ol and nitric acid aqueous solution. This mixture resulted in a one-phase medium, which was indefinitely stable. No changes in the analyte signals were observed over several days in spiked samples, proving long-term stabilization ability. The use of conventional (Pd) and permanent (Ir) modification was investigated and the former was preferred. Central composite design multivariate optimization defined the optimum microemulsion composition as well as the temperature program. In this way, calibration using aqueous analytical solutions was possible, since the same sensitivity was observed in the investigated microemulsion media and in 0.2% v/v HNO(3). Coefficients of correlation larger than 0.999 and an As characteristic mass of 22 pg were observed. Recoveries (n=4) obtained from spiked samples were 98+/-4, 99+/-3 and 103+/-5%, and the limits of detection in the original samples were 1.8, 1.2 and 1.5 microg L(-1) for diesel, gasoline and naphtha, respectively. Validation was performed by the analysis of a set of commercial samples by independent comparative procedures. No significant difference (Student's t-test, p<0.05) was observed between comparative and proposed procedure results. The total determination cycle lasted 4 min for diesel and 3 min for gasoline and naphtha, equivalent to a sample throughput of 7 h(-1) for diesel and 10 h(-1) for gasoline and naphtha.

Muscular tissue from wild-caught mullet (Mugil spp.) and snook (Centropomus spp.)

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