ABSTRACT: Mercury-resistant bacteria isolated from soil samples contaminated with mercury released from artisanal gold processing sites in Sukabumi, Indonesia
Project description:Effects of mercury contamination on microbial abundance and diversity in Amazon ecosystems disturbed by artisanal and small-scale gold mining
Project description:The consistent cold temperatures and large amount of precipitation in the Olympic and Cascade ranges of Washington State are thought to increase atmospheric deposition of contaminants in these high elevation locations. Total mercury and 28 organochlorine compounds were measured in composite, whole fish samples collected from 14 remote lakes in the Olympic, Mt. Rainer, and North Cascades National Parks. Mercury was detected in fish from all lakes sampled and ranged in concentration from 17 to 262 ug/kg wet weight. Only two organochlorines, total polychlorinated biphenyls (tPCB) and dichlorodiphenyldichloroethylene (DDE), were detected in fish tissues (concentrations <25 ug/kg wet weight). No organochlorines were detected in sediments (MRL ≈1-5 ug/kg), while median total and methyl mercury in sediments were 30.4 and 0.34 ug/kg (dry weight), respectively. Using a targeted rainbow trout cDNA microarray with known genes, we detected significant differences in liver transcriptional responses, including metabolic, endocrine, and immune-related genes, in fish collected from a contaminated lake compared to a lake with a lower contaminant load. Overall, our results suggest that local urban areas are contributing to the observed contaminant patterns, while the transcriptional changes point to a biological response associated with exposure to these contaminants in fish. Specifically, the gene expression pattern leads us to hypothesize a role for mercury in disrupting the metabolic and reproductive pathways in fish from high elevation lakes in western Washington. Keywords: High altitude lakes, mercury, salmonids, organochlorines
Project description:Epidemiological studies link exposure to mercury with autoimmune disease. Unfortunately, in spite of considerable effort, no generally accepted mechanistic understanding of how mercury actually functions with respect to the etiology of autoimmune disease is currently available. Nevertheless, autoimmune disease often arises because of defective B cell signaling. Because B cell signaling is dependent on phosphorylation cascades, in this report, we have focused on how mercury intoxication alters phosphorylation of B cell proteins in antigen-non stimulated (tonic) mouse splenic B cells. Specifically, we utilized mass spectrometric techniques to conduct a comprehensive unbiased global analysis of the effect of mercury on the entire B cell phosphoproteome. We found that the effects were pleotropic in the sense that large numbers of pathways were impacted. However, confirming our earlier work, we found that the B cell signaling pathway stood out from the rest, in that phosphoproteins which had sites which were affected by mercury, exhibited a much higher degree of connectivity, than components of other pathways. Further analysis showed that many of these BCR pathway proteins had been previously linked to autoimmune disease. Finally, dose response analysis of these BCR pathway proteins showed STIM1_S575, and NFAT2_S259 are the two most mercury sensitive of these sites. Because STIM1_S575 controls the ability of STIM1 to regulate internal Ca2+, we speculate that STIM1 may be the initial point of disruption, where mercury interferes with B cell signaling leading to systemic autoimmunity, with the molecular effects pleiotropically propagated throughout the cell by virtue of Ca2+ dysregulation.
2024-10-17 | PXD042189 | Pride
Project description:Cd-resistant bacteria isolated from Cd-Contaminated Mining Areas
Project description:Gold salts has been used in the treatment of rheumatoid arthritis but has been replaced by biologicals such as TNF-alpha inhibitors. The mechanisms behind the anti-inflammatory effect of metallic gold ions are still unknown, however, recent data showed that charged gold atoms are released from pure metallic gold implants by macrophages via a dissolucytosis membrane, and that gold ions are taken up by local macrophages, mast cells and to some extent fibroblasts. These current findings offer new treatment options for metallic gold and deeper understanding of the effect of metallic gold on key inflammatory cells as macrophages are essential. In the present study the impact of phagocytised gold ions on the global gene expression profile of the human monocytic cell line THP-1 was investigated, using microarray analysis comprising approximately 20,000 genes. The gene expression data was confirmed by measurement of three secreted proteins. A unique gene expression signature of dissolucytotic macrophages that had taken up gold ions was demonstrated. A large number of regulated genes were functionally related to immunomodulation/protection. Gold ion uptake into macrophages induced downregulation of central inflammatory cytokines as TNF-alpha, IL-32 and CD28. The data obtained in this study offer new insights into the mode of action of gold ions and suggest a future role of metallic gold as implants or topical applications in treating inflammation. To determine the effect of gold phagocytosis on global gene expression