Modern classification of the family of human small heat shock proteins (the so-called HSPB) is presented, and the structure and properties of three members of this family are analyzed in detail. Ub...

Large Potentials of Small Heat Shock Proteins

Detection of environmental contamination such as trace-level toxic heavy metal ions mostly relies on bulky and costly analytical instruments. However, a considerable global need exists for portable, rapid, specific, sensitive, and cost-effective detection techniques that can be used in resource-limited and field settings. Here we introduce a smart-phone-based hand-held platform that allows the quantification of mercury(II) ions in water samples with parts per billion (ppb) level of sensitivity. For this task, we created an integrated opto-mechanical attachment to the built-in camera module of a smart-phone to digitally quantify mercury concentration using a plasmonic gold nanoparticle (Au NP) and aptamer based colorimetric transmission assay that is implemented in disposable test tubes. With this smart-phone attachment that weighs <40 g, we quantified mercury(II) ion concentration in water samples by using a two-color ratiometric method employing light-emitting diodes (LEDs) at 523 and 625 nm, where a cus...

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Detection and spatial mapping of mercury contamination in water samples using a smart-phone.

Oxidative stress and metal carcinogenesis.

The heavy metals mercury and lead are well-known and significant developmental neurotoxicants. This review summarizes the genetic factors that modify their toxicokinetics. Understanding toxicokinetics (uptake, biotransformation, distribution, and elimination processes) is a key precondition to understanding the individual health risks associated with exposure. We selected candidate susceptibility genes when evidence was available for (1) genes/proteins playing a significant role in mercury and lead toxicokinetics, (2) gene expression/protein activity being induced by these metals, and (3) mercury and lead toxicokinetics being affected by gene knockout/knockdown or (4) by functional gene polymorphisms. The genetic background is far better known for mercury than for lead toxicokinetics. Involved are genes encoding L-type amino acid transporters, organic anion transporters, glutathione (GSH)-related enzymes, metallothioneins, and transporters of the ABC family. Certain gene variants can influence mercury toxicokinetics, potentially explaining part of the variable susceptibility to mercury toxicity. Delta-aminolevulinic acid dehydratase ( ALAD ), vitamin D receptor ( VDR ) and hemochromatosis ( HFE ) gene variants are the only well-established susceptibility markers of lead toxicity in humans. Many gaps remain in our knowledge about the functional genomics of this issue. This calls for studies to detect functional gene polymorphisms related to mercury- and lead-associated disease phenotypes, to demonstrate the impact of functional polymorphisms and gene knockout/knockdown in relation to toxicity, to confirm the in vivo relevance of genetic variation, and to examine gene–gene interactions on the respective toxicokinetics. Another crucial aspect is knowledge on the maternal-fetal genetic background, which modulates fetal exposure to these neurotoxicants. To completely define the genetically susceptible risk groups, research is also needed on the genes/proteins involved in the toxicodynamics, i.e., in the mechanisms causing adverse effects in the brain. Studies relating the toxicogenetics to neurodevelopmental disorders are lacking (mercury) or very scarce (lead). Thus, the extent of variability in susceptibility to heavy metal-associated neurological outcomes is poorly characterized.

Ilaria Schena

Papers

Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead.

Different role of Schisandrin B on mercury-induced renal damage in vivo and in vitro