Effects of soft electrophiles on selenium physiology.

This review examines the effects of neurotoxic electrophiles on selenium (Se) metabolism. Selenium-dependent enzymes depend on the unique and elite functions of selenocysteine (Sec), the 21st proteinogenic amino acid, to perform their biochemical roles. Humans possess 25 selenoprotein genes, ~ half of which are enzymes (selenoenzymes) required for preventing, controlling, or reversing oxidative damage, while others participate in regulating calcium metabolism, thyroid hormone status, protein folding, cytoskeletal structure, Sec synthesis and Se transport.

Umbilical cord blood and placental mercury, selenium and selenoprotein expression in relation to maternal fish consumption.

Seafood is an important source of nutrients for fetal neurodevelopment. Most individuals are exposed to the toxic element mercury through seafood. Due to the neurotoxic effects of mercury, United States government agencies recommend no more than 340g (12oz) per week of seafood consumption during pregnancy.

Seafood consumption and umbilical cord blood mercury concentrations in a multiethnic maternal and child health cohort.

Background: Fish consumption is common among the cultures of Hawaii, and given public health attention to mercury exposure in pregnancy, it is important to better understand patterns of fish consumption and mercury in pregnancy. This study examined the influence of maternal fish consumption during pregnancy on umbilical cord mercury (Hg) concentrations in a multiethnic cohort of women in Hawaii.

Methods: This secondary analysis of a prospective cohort pilot study examined antenatal seafood consumption and neonatal outcomes in Hawaii.

Potential Role of Selenoenzymes and Antioxidant Metabolism in relation to Autism Etiology and Pathology.

Autism and autism spectrum disorders (ASDs) are behaviorally defined, but the biochemical pathogenesis of the underlying disease process remains uncharacterized. Studies indicate that antioxidant status is diminished in autistic subjects, suggesting its pathology is associated with augmented production of oxidative species and/or compromised antioxidant metabolism. This suggests ASD may result from defects in the metabolism of cellular antioxidants which maintain intracellular redox status by quenching reactive oxygen species (ROS).

The nail as a noninvasive indicator of methylmercury exposures and mercury/selenium molar ratios in brain, kidney, and livers of Long-Evans rats.

Animal studies indicate that the toxic effects of methylmercury (MeHg) exposures increase when selenium (Se) status is low. Toxicity is directly proportional to Hg/Se molar ratios in critical tissues such as brain and increase dramatically as molar ratios exceed 1:1. In this study, we examined the nail as a biomonitor of Hg/Se molar ratios in kidney, liver, and brain tissues of weanling male Long-Evans rats fed controlled diets containing varying amounts of Se and MeHg.

Dietary selenium's protective effects against methylmercury toxicity.

Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity. Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets. Although these effects have been known since 1967, they have only lately become well understood.

How might selenium moderate the toxic effects of mercury in stream fish of the western U.S.?

The ability of selenium (Se) to moderate mercury (Hg) toxicity is well established in the literature. Mercury exposures that might otherwise produce toxic effects are counteracted by Se, particularly when Se:Hg molar ratios approach or exceed 1. We analyzed whole body Se and Hg concentrations in 468 fish representing 40 species from 137 sites across 12 western U.

Selenium health benefit values as seafood safety criteria.

Selenium (Se) is absolutely required for activity of 25-30 genetically unique enzymes (selenoenzymes). All forms of life that have nervous systems possess selenoenzymes to protect their brains from oxidative damage. Homeostatic mechanisms normally maintain optimal selenoenzyme activities in brain tissues, but high methylmercury (MeHg) exposures sequester Se and irreversibly inhibit selenoenzyme activities.

Mercury toxicity and the mitigating role of selenium.

Mercury is a well-known environmental toxicant, particularly in its most common organic form, methylmercury. Consumption of fish and shellfish that contain methylmercury is a dominant source of mercury exposure in humans and piscivorous wildlife. Considerable efforts have focused on assessment of mercury and its attendant risks in the environment and food sources, including the studies reported in this issue.

Dietary and tissue selenium in relation to methylmercury toxicity.

Selenium (Se) supplementation in the nutritionally relevant range counteracts methylmercury (MeHg) toxicity. Since Se tends to be abundant in fish, MeHg exposures alone may not provide an accurate index of risk from fish consumption. Molar ratios of MeHg:Se in the diets and Hg:Se in tissues of exposed individuals may provide a more accurate index.

Importance of molar ratios in selenium-dependent protection against methylmercury toxicity.

The influence of dietary selenium (Se) on mercury (Hg) toxicity was studied in weanling male Long Evans rats. Rats were fed AIN-93G-based low-Se torula yeast diets or diets augmented with sodium selenite to attain adequate- or rich-Se levels (0.1, 1.

Selenium and mercury in pelagic fish in the central north pacific near Hawaii.

Protective effects of selenium against mercury toxicity have been demonstrated in all animal models evaluated. As interactions between selenium and mercury and their molar ratios in seafood are essential factors in evaluating risks associated with dietary mercury exposure, considering mercury content alone is inadequate. In this study, the absolute and molar concentrations of mercury and selenium were determined in edible portions from 420 individual fish representing 15 species of pelagic fish collected from the central North Pacific Ocean near Hawaii.

The roles of selenium and mercury in the pathogenesis of viral cardiomyopathy.

Research on the pathogenesis of nonischemic dilated cardiomyopathy (DCM) has largely been focused on the role of viral pathogens and altered immunity. Trace elements have only rarely been considered; however, clinical observations that trace elements influence cardiovascular disease have been made in populations with extreme dietary deficiency or occupational exposure. Recently, animal models of DCM have been used to explore interactions among trace elements, viral pathogens, and the immune system.

Transmembrane partitioning of boron and other elements in RAW 264.7 and HL60 cell cultures.

The trace element boron is essential for all higher plants and is beneficial or has been established as essential for several animal models of human nutrition. To help identify the biomolecules that require boron for function in humans, we determined whether intracellular boron is retained against a concentration gradient. Cells (Abelson leukemia virus BALB murine monocyte-macrophage RAW 264.

Contrasting and cooperative effects of copper and iron deficiencies in male rats fed different concentrations of manganese and different sources of sulfur amino acids in an AIN-93G-based diet.

Dietary nutrient interactions are important factors to consider in the study of nutrient status and requirements. Here, the effects of dietary interactions among copper (Cu), iron (Fe), manganese (Mn) and sulfur amino acids (SAA) on blood cell characteristics and enzyme activities were observed. Male rats (n = 8) were used in a 2 x 2 x 2 x 2 factorial design and fed an AIN-93G-based diet containing dietary Cu (<1 and 5 mg/kg), Fe (10 and 35 mg/kg), Mn (10 and 50 mg/kg) and either L-cystine (LCys) or DL-methionine (DLMet).