Regional assessment of the historical trends of mercury in sediment cores from Wider Caribbean coastal environments.

Spatial and temporal variations of mercury (Hg) concentrations, enrichment, and potential ecological risks were studied in a suite of lead-210 (210Pb) dated sediment cores from 13 Wider Caribbean Region coastal environments. Broad variability of Hg concentrations (19-18761 ng g-1) was observed, encompassing even background levels (38-100 ng g-1). Most Hg concentration profiles exhibited a characteristic upward trend, reaching their peak values in the past two decades. Most of the sediment sections, showing from moderately to very severe Hg enrichment, were found in cores from Havana Bay and Sagua River Estuary (Cuba), Port-au-Prince Bay (Haiti), and Cartagena Bay (Colombia). These were also the most seriously contaminated sites, which can be considered regional Hg 'hotspots'. Both Havana Bay and Port-au-Prince Bay reportedly receive waste from large cities with populations exceeding 2 million inhabitants, and watersheds affected by high erosion rates. The records from the Sagua River Estuary and Cartagena Bay reflected historical Hg contamination associated with chloralkali plants, and these sites are of very high ecological risk. These results constitute a major contribution to the scarce regional data on contaminants in the Wider Caribbean Region and provide reference information to support the evaluation of the effectiveness of the Minamata Convention.

High glucose concentrations induce oxidative stress by inhibiting Nrf2 expression in rat Müller retinal cells in vitro.

Diabetic retinopathy (DR) is a complication of diabetes. Several studies have implicated oxidative stress as a fundamental factor in the progression of the disease. The nuclear factor erythroid-2-related factor 2 (Nrf2) is one of the main regulators of redox homeostasis. Glia Müller cells (MC) maintain the structural and functional stability of the retina. The objective of this study was to evaluate the effect of high glucose concentrations on reactive oxygen species (ROS) production and Nrf2 expression levels in rat MC. MC were incubated with normal (NG; 5 mM) or high glucose (HG; 25 mM) for different times. Incubation with HG increased ROS levels from 12 to 48 h but did not affect cell viability. However, exposure to 3 h of HG caused a transient decrease Nrf2 levels. At that time, we also observed a decrease in the mRNA expression of Nrf2 target genes, glutathione levels, and catalase activity, all of which increased significantly beyond initial levels after 48 h of incubation. HG exposure leads to an increase in the p65 subunit of nuclear factor-κB (NF-kB) levels, and its target genes. These results suggest that high glucose concentrations lead to alteration of the redox regulatory capacity of Nrf2 mediated by NF-kB regulation.

Retinal Nrf2 expression in normal and early streptozotocin-diabetic rats.

Diabetic retinopathy is the most common cause of vision loss among diabetic patients. Although hyperglycemia produces retinal oxidative stress in long-standing diabetes, the pathogenesis mechanism is unknown. The Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a central role in cell responses against oxidative damage. We used adult Long Evans rats where diabetes was induced by streptozotocin. Normal and treated rats were sacrificed at 7, 20, and 45 days after streptozotocin injection. We analyzed Nrf2 and Keap1 expression in retinal homogenates, cytoplasmic, and nuclear retinal fractions. Normal retina showed Nrf2 expression in all retina nuclear layers. We found a transitory decrease of Nrf2 mRNA and protein expression at 7 and 20 days after the streptozotocin injection that recovered later on: moreover, the protein level increased after 45 days. Keap1 immunoprecipitation revealed similar levels as Nrf2 in normal and diabetic rat retinas, indicating that the diabetic condition did not lead to dissociation of the Keap1-Nrf2 complex. Indeed, glutathione levels and superoxide dismutase activity were not altered in the treated rat retinas. These results do not support oxidative stress in the retina shortly after diabetes induction.