Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs). A wide variety of pathologic alterations occur in animals and humans with Se-E deficiency. Myocardial lesions are seen most frequently in calves, lambs, pigs, turkey poults, and ducklings. In humans, Keshan disease, an endemic cardiomyopathy in China, is attributed to Se deficiency. Necrosis of skeletal muscle is the most frequent lesion observed in animal species. Necrosis of smooth muscle of the gizzard and intestine may be a prominent lesion in turkey poults, ducklings, and quail. Other Se-E deficiency lesions include hepatic necrosis, gastric ulceration, intestinal and uterine lipofuscinosis, pancreatic damage, steatitis, exudative diathesis, encephalomalacia, and testicular necrosis. Selenium toxicosis is well characterized in animals and humans by neurological, hoof, and hair alterations.     

Effects of excess selenomethionine on selenium status indicators in pregnant long-tailed macaques (Macaca fascicularis)

Forty pregnant long-tailed macaques were treated daily for 30 d with 0, 25, 150 or 300 μg selenium as L-selenomethionine/kg body weight. Erythrocyte and plasma selenium and glutathione peroxidase specific activities, hair and fecal selenium, and urinary selenium excretion were increased by and were linearly related to L-selenomethionine dose. Hair selenium was most sensitive to L-selenomethionine dose, with an 84-fold increase in the 300 μg selenium/(kg-d) group relative to controls (r=0.917). Daily urinary selenium excretion (80-fold,r=0.958), plasma selenium (22-fold,r=0.885), erythrocyte selenium (24-fold,r=0.920), and fecal selenium (18-fold,r=0.911) also responded strongly to L-selenomethionine. Erythrocyte and plasma glutathione peroxidase specific activities increased 154% and 69% over controls, respectively. Toxicity was associated with erythrocyte selenium >2.3 μg/mL, plasma selenium >2.8 μg/mL, and hair selenium >27 μg/g. Plasma, erythrocyte, and hair selenium concentrations may be useful for monitoring and preventing the toxicity of L-selenomethionine administered to humans in cancer chemoprevention trials.     

Effects of autoclave-induced carbohydrate hydrolysis on the growth ofBeta vulgaris cells in suspension

Media of de Greef & Jacobs (1979) were autoclaved either with all the nutrient components in a single vessel (medium 1) or with the following components in separate vessels: FeNa–EDTA+CaCl₂ (medium 2), FeNa–EDTA+NaH₂PO₄ (medium 3) or sucrose (medium 4). Medium 5 was prepared by autoclaving FeNa–EDTA+NaH₂PO₄ and sucrose in two separate vessels. It was found that the dry mass yield of cell suspensions ofBeta vulgaris was lowest in medium 1, followed by media 2 and 3. There was no significant difference among media 3, 4, and 5.The plot of dry mass yield of the cell suspensions against the rates of cyanide-initiated oxygen consumption which indicate the extent of carbohydrate hydrolysis of the media during autoclaving, indicated the presence of a threshold rate of about 17–20 nmol ml^–1 min^–1. Dry mass yield of the suspensions decreased rapidly when the rate exceeded this value.For media with glucose as the source of carbohydrate, the rate of cyanide-initiated oxygen consumption exceeded the threshold value by a factor of 1.5 to 2, depending on the volume of the media autoclaved.Abbreviations FeNa-EDTA ferric monosodium ethylenediamine-tetraacetic acid     

Effect of heavy metals on isoperoxidases of Wheat

The influence of increasing concentrations of copper, zinc, lead, nickel, chromium and cadmium on 14-day-old seedlings of wheat (Triticum aestivum L. cv. Vergina) was studied. Plants were grown in 1/10 strength Rorison’s nutrient solution with increasing concentrations of each of the metals added separately. The toxicity of metals depressed shoot growth but the most evident symptoms were on roots. The concentration of each metal which caused inhibition of root growth was chosen to study the influence of metals on isoperoxidases of wheat shoots. The concentrations employed did not alter the number of peroxidase bands but almost in all cases enhanced the intensities of bands of pH 4.0-4.2 and 5.0-5.4, while they decreased the intensities of bands of pH 4.2-4.6 and 5.4-6.5. The similar effects of the different heavy metals employed may suggest similarity in metal action on wheat isoperoxidases. The increased intensities of peroxidase bands may be considered as an indication of enhanced senescence caused by the heavy metal treatments. Generally, our results suggest that the heavy metals employed have caused complex changes on the multiple forms of peroxidases.     

Strategies for reducing solvent toxicity in extractive fermentations

The toxicity of an Alamine 336/oleyl-alcohol extraction system on Lactobacillus delbrueckii was investigated. It was shown that the solvent affected the cells through the water-soluble portion and the immiscible portion of the solvent. While immobilization significantly protected the cells from the immiscible solvent phase, the water-soluble part of the solvent still caused toxicity to the microorganisms due to diffusion of the solvent into the matrix. Adding soybean oil to the kappa-carrageenan matrix could trap the diffusing solvent molecules, and therefore reduce the toxic effect from the water soluble portion of the solvent. The protective ability of soybean oil was quantified through mathematical modeling and experimentation.     

Application of cell culture toxicity tests to the development of implantable biosensors

Cell culture toxicity testing methods were modified and applied to the development of implantable glucose microsensors, and positive and negative control materials suitable for the microsensor assessment were established. The location, source and degree of the toxic effect in a multi-component biosensor was spatially visualized with cell monolayers. A freshly prepared sensor showed moderate toxicity, mainly as a result of the presence of glutaraldehyde and the residual solvents in the polymer layers. However, it was possible to reduce the toxicity by removing the leachable toxic substances through extraction in phosphate, buffer, and a non-toxic sensor was readily obtained.     

Sorption of hydrophobic organic contaminants and trace metals on phytoplankton and implications for toxicity assessment

The partitioning of trace metals and hydrophobic organic contaminants to phytoplankton determines their toxicity as well as their fate and transport in aquatic ecosystems. Accurate impact assessments, therefore, depend on a good understanding of the factors regulating the sorption of these compounds to biotic particles. The accumulation of chlorinated organic compounds in phytoplankton is generally considered as being due solely to physical sorption, described by reversible equilibrium models based on Langmuir or Freundlich isotherms. On the other hand, the uptake of trace metals is a two phase process: a fast sorption component viewed as an ionexchange or a covalent bonding process with cell surface ligands, followed by an intracellular transport phase that is dependent on cellular metabolic activity. The uptake of inorganic and hydrophobic organic pollutants and their bioaccumulation are influenced in a complex manner by duration of exposure and cell density, by environmental factors such as pH, the concentration of cations and of dissolved and colloidal organic matter, as well as by phytoplankton physiological condition. High concentrations of H⁺, Ca²⁺, and Mg²⁺ ions will reduce trace metal sorption by directly competing for uptake sites on the cell's surface, whereas the presence of dissolved organic carbon such as natural and synthetic chelators and phytoplankton exudates will reduce the bioavailability of both trace metals and hydrophobic organic contaminants. Thus, the impact of toxic contaminants on phytoplankton may be determined as much by the factors influencing uptake and partitioning as by the potency of the toxicants and interspecies differences in sensitivity. Recommendations for improving toxicity assessments are presented.     

Ecosystem health as measured from the molecular to the community level of organization,with reference to sediment bioassessment

The current recognition that chemical measurements are uncertain indicators of biological consequences of pollution has shifted the emphasis away from assessing environmental chemistry alone toward the inclusion of measurements of the health of organisms. Effects of pollutants begin with the individual, have subsequent repercussions on population level processes, and ramifications for community structure and functions. Pollutants act at a molecular level and the biochemical lesions is the first step in the manifestation of effects. Technologies that operate at the cellular level assist in elucidating toxicity. Higher levels of integration include an organism's capacity for growth. Laboratory bioassays andin situ research can monitor physiological incapacities and assist in predicting population level effects. A yet higher level of organization is that of the ecological community.