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PubMed1987

The infected hairs of tinea capitis due to Microsporum canis: demonstration of uniqueness of the hair cuticle by scanning electron microscopy.

Scanning and transmission electron microscopic studies were done on scalp hairs of four patients infected with ectothrix Microsporum canis. Both freeze fracture and cross-sectioning of hairs revealed a thick sheath of fungal spores encircling the hair shaft beneath an intact cuticle. These spores were not visible on surface inspection but became apparent only where the cuticle had been rubbed off or broken. Daily selenium sulfide shampoos removed all of the spores from these sites. The cuticle is viewed as being an effective barrier to the penetration of fungi, so that the hair is vulnerable to fungus infection only deep within the hair follicle below the level of the mature cuticle. Once the fungus enters the hair cortex just above the hair bulb, it produces myriads of spores that remain trapped and hidden beneath the cuticle for the length of the intact hair.

Child↗
PubMed1996

Study of mercury-selenium (Hg-Se) interactions and their impact on Hg uptake by the radish (Raphanus sativus) plant.

Pot culture experiments were conducted to study the effects of selenite and selenate treatment (0.5-6.0 microg/ml) on the uptake and translocation of root-absorbed mercury (Hg) in radish plants irrigated with 2 and 5 microg/ml Hg in sand and soil culture. Statistically significant reductions in mercury uptake with increasing concentrations of selenium (Se) were observed. Both forms of selenium (selenite and selenate) were equally effective in reducing the mercury burden of the plant. The observed reduction in plant uptake of mercury is explained by the formation of an HgSe insoluble complex in the soil-root environment. No significant difference (P > 0.05) in dry matter yields with the various selenium treatments was found, suggesting that no selenium toxicity or salt injury occurred in the plants.

Drug Interactions↗
PubMed1997

Mouse strain and source of L-tryptophan affects hepatic nuclear tryptophan binding.

This study describes that the affinity for specific L-tryptophan binding to hepatic nuclei in vitro is markedly decreased in NZBWF1 mice in comparison to that in Swiss mice. Also, the hepatic nuclei of NZBWF1 mice have a significantly decreased binding response in vitro to Showa Denko L-tryptophan (implicated in the eosinophilia-myalgia syndrome) or to its contaminants, 1,1'-ethylidenebis(tryptophan) or 3-phenylamino-L-alanine, when each is added to control, non-implicated L-tryptophan compared with hepatic nuclei of Swiss mice. Enhanced hepatic protein synthesis induced by tube-feeding control L-tryptophan is much less in NZBWF1 mice than in Swiss mice. Tube-feeding of Showa Denko L-tryptophan induced less stimulation of hepatic protein synthesis than did control L-tryptophan in Swiss mice but essentially none in NZBWF1 mice. NZBWF1 mice have a genetically altered response to L-tryptophan which may prove to be useful is studying the role of L-tryptophan in health and in disease.

Alanine↗
PubMed2001

Inhibitory zinc-enriched terminals in mouse spinal cord.

The ultrastructural localization of zinc transporter-3, glutamate decarboxylase and zinc ions in zinc-enriched terminals in the mouse spinal cord was studied by zinc transporter-3 and glutamate decarboxylase immunohistochemistry and zinc selenium autometallography, respectively. The distribution of zinc selenium autometallographic silver grains, and zinc transporter-3 and glutamate decarboxylase immunohistochemical puncta in both ventral and dorsal horns as seen in the light microscope corresponded to their presence in the synaptic vesicles of zinc-enriched terminals at ultrastructural levels. The densest populations of zinc-enriched terminals were seen in dorsal horn laminae I, III and IV, whereas the deeper laminae V and VI contained fewer terminals. At ultrastructural levels, zinc-enriched terminals primarily formed symmetrical synapses on perikarya and dendrites. Only relatively few asymmetrical synapses were observed on zinc-enriched terminals. In general, the biggest zinc-enriched terminals contacted neuronal somata and large dendritic elements, while medium-sized and small terminals made contacts on small dendrites. The ventral horn was primarily populated by big and medium-sized zinc-enriched terminals, whereas the dorsal horn was dominated by medium-sized and small zinc-enriched terminals. The presence of boutons with flat synaptic vesicles with zinc ions and symmetric synaptic contacts suggests the presence of inhibitory zinc-enriched terminals in the mammalian spinal cord, and this was confirmed by the finding that zinc ions and glutamate decarboxylase are co-localized in these terminals. The pattern of zinc-enriched boutons in both dorsal and ventral horns is compatible with evidence suggesting that zinc may be involved in both sensory transmission and motor control.

Animals↗
PubMed2003

Selenate reduction by Enterobacter cloacae SLD1a-1 is catalysed by a molybdenum-dependent membrane-bound enzyme that is distinct from the membrane-bound nitrate reductase.

Enterobacter cloacae SLD1a-1 is capable of reducing selenium oxyanions to elemental selenium under both aerobic and anaerobic conditions. In this study the enzyme that catalyses the initial reduction of selenate (SeO4(2-)) to selenite (SeO3(2-)) has been localised to isolated cytoplasmic membrane fractions. Experiments with intact cells have shown that the putative selenate reductase can accept electrons more readily from membrane-impermeable methyl viologen than membrane-permeable benzyl viologen, suggesting that the location of the catalytic site is towards the periplasmic side of the cytoplasmic membrane. Enzyme activity was enhanced by growing cells in the presence of 1 mM sodium molybdate and significantly reduced in cells grown in the presence of 1 mM sodium tungstate. Non-denaturing polyacrylamide gel electrophoresis (PAGE) gels stained for selenate and nitrate reductase activity have revealed that two distinct membrane-bound enzymes catalyse the reduction of selenate and nitrate. The role of this membrane-bound molybdenum-dependent reductase in relation to selenate detoxification and energy conservation is discussed.

Benzyl Viologen↗
PubMed2001

Speciation and metabolism of selenium injected with 82Se-enriched selenite and selenate in rats.

Selenate and selenite injected intravenously into rats were speciated by the HPLC-ICP MS method with use of an enriched stable isotope as the tracer. In dose-relation experiments, 82Se-enriched selenate or selenite was injected intravenously into male Wistar rats of 8 weeks of age (three rats/group) at single doses of 10, 25, 50, 100 and 200 microg/kg body weight for the selenate group, and 2, 5, 10, 25 and 50 microg/kg body weight for the selenite group. The animals were sacrificed 1 or 24 h later, and the concentrations and distributions of 82Se in the liver, kidneys, serum, and urine remaining in the bladder or 24-h urine were determined. In time-course experiments, 82Se-enriched selenate and selenite were injected at doses of 50 and 10 microg/kg body weight, respectively, and the animals were sacrificed 5, 15, 30, 60 and 180 min later. It was suggested that selenate is directly taken up by the liver with an efficiency of approximately 1/2 compared with selenite, the latter being taken up by the liver after being metabolized to selenide in red blood cells. Although selenate and selenite were metabolized differently in the bloodstream, and also a part of only selenate was excreted directly into the urine, the 82Se taken up by the liver was shown to be metabolized in a manner indistinguishable between selenate and selenite. 82Se of selenite origin but not of selenate origin was suggested to undergo redox reaction in the bloodstream. These results suggest that although parenteral selenate is utilized less efficiently by the body, it is utilized in the liver in a similar manner to selenite much more safely.

Animals↗
PubMed2000

Respiration of arsenate and selenate by hyperthermophilic archaea.

A novel, strictly anaerobic, hyperthermophilic, facultative organotrophic archaeon was isolated from a hot spring at Pisciarelli Solfatara, Naples, Italy. The rod-shaped cells grew chemolithoautotrophically with carbon dioxide as carbon source, hydrogen as electron donor and arsenate, thiosulfate or elemental sulfur as electron acceptor. H2S was formed from sulfur or thiosulfate, arsenite from arsenate. Organotrophically, the new isolate grew optimally in the presence of an inorganic electron acceptor like sulfur, selenate or arsenate. Cultures, grown on arsenate and thiosulfate or arsenate and L-cysteine, precipitated realgar (As2S2). During growth on selenate, elemental selenium was produced. The G+C content of the DNA was 58.3 mol%. Due to 16S rRNA gene sequence analysis combined with physiological and morphological criteria, the new isolate belongs to the Thermoproteales order. It represents a new species within the genus Pyrobaculum, the type species of which we name Pyrobaculum arsenaticum (type strain PZ6*, DSM 13514, ATCC 700994). Comparative studies with different Pyrobaculum-species showed, that Pyrobaculum aerophilum was also able to grow organotrophically under anaerobic culture conditions in the presence of arsenate, selenate and selenite. During growth on selenite, elemental selenium was formed as final product. In contrast to P. arsenaticum, P. aerophilum could use selenate or arsenate for lithoautotrophic growth with carbon dioxide and hydrogen.

Anaerobiosis↗
PubMed2000

Chromosome damage induced by selenium salts in human peripheral lymphocytes.

Two inorganic salts of selenium, sodium selenite (Na(2)SeO(3)) and sodium selenate (Na(2)SeO(4)), were screened for damage to chromosome and cell division following exposure to human lymphocyte cultures. In vitro exposure of human peripheral blood lymphocytes to high concentration of two inorganic salts of selenium-sodium selenite (2.9 x 10(-5) M) and sodium selenate (2.65 x 10(-5) M)-was found to be lethal; no blast cells being formed. Lower concentrations of both salts, 5.8 x 10(-6) M and 1.06 x 10(-5) M, respectively, were highly mitostatic. Lower concentrations of sodium selenite (2.9 x 10(-6) M, 1.16 x 10(-6) M and 2.32 x 10(-7) M) and sodium selenate (5.3 x 10(-6) M, 2.65 x 10(-6) M and 1.06 x 10(-6) M), respectively, induced chromosomal aberrations and reduced cell division in proportions directly related to the dose. Sodium selenite was considerably more clastogenic than sodium selenate.

Adult↗
PubMed1999

Possible involvement of thioredoxin reductase as well as thioredoxin in cellular sensitivity to cis-diamminedichloroplatinum (II).

The thioredoxin (TRX) system, composed of nicotinamide adenine dinucleotide phosphate (reduced form), TRX, and TRX reductase (TRXR), has multiple biologic functions via thiol-mediated redox control. In this study, we investigated the relationship between intracellular TRXR levels and cellular sensitivity to cis-diamminedichloroplatinum (II) (CDDP). HeLa, a human cervical carcinoma cell line, cultured with CDDP showed a time- and dose-dependent reduction of intracellular TRXR activity, which was well correlated with the decrease in cell viability after exposure to CDDP. In a cell-free system, CDDP was found to directly inactivate the reduced form of purified human TRXR. The CDDP-resistant variants of HeLa cells, established by continuous exposure to CDDP, exhibited an increased expression and activity of TRXR as well as TRX compared with the parental cells. In addition, sodium selenate, an inhibitor of TRXR, was found to increase the susceptibility to CDDP in the CDDP-resistant cells. Moreover, the HeLa cells transfected with an antisense TRXR RNA expression vector to reduce the intracellular enzyme activity displayed an enhanced sensitivity to CDDP. Taken together with previous reports on TRX, these results indicate the possible involvement of TRXR as well as TRX in the cellular sensitivity and resistance to CDDP.

Antineoplastic Agents↗
PubMed1999

1,3-Selenazine derivatives induce cytotoxicity and DNA fragmentation in human HT-1080 fibrosarcoma cells.

The inhibitory effects of a series of 5,6-dihydro-4H-1,3-selenazine derivatives, 1,3-selenazole, and 5,6-dihydro-4H-1,3-thiazine derivatives on the proliferation of human HT-1080 fibrosarcoma cells were investigated. The compounds 4-ethyl-4-hydroxy-2-p-tolyl-5, 6-dihydro-4H-1,3-selenazine (TS-2) and 4-hydroxy-4-methyl-6-propyl-2-p-tolyl-5,6-dihydro-4H-1,3-selenazine++ + (TS-6) exhibited the strongest inhibitory effect among 1, 3-selenazine derivatives, and the EC(50) of TS-2 and TS-6 was 7.76 and 8.40 microM, respectively. On the other hand, 1,3-selenazole and 5,6-dihydro-4H-1,3-thiazines had no inhibitory effects. TS-2 and TS-6 inhibited the proliferation of HT-1080 cells time- and dose-dependently. They induced dose-dependent DNA fragmentation in HT-1080 cells, revealing a typical apoptosis characteristics. The present study demonstrated that TS-2 and TS-6 inhibited HT-1080 proliferation through the induction of DNA fragmentation.

Apoptosis↗
PubMed1995

Human selenium supplementation as assessed by changes in blood selenium concentration and glutathione peroxidase activity.

This review concentrates on the differences in the effects on indicators of selenium (Se) status of different chemical forms proposed for Se supplementation in healthy subjects. Modifications in blood (plasma and erythrocyte) Se concentrations and in the Se-dependent glutathione peroxidase (GSH-Px) enzymatic activity, in plasma, erythrocytes and platelets, were compared considering the basal Se status, the dose and the chemical form of Se supplement, as well as the duration of the intervention. Organic Se forms (Se-yeast, selenomethionine and food-Se) increased blood Se more concentration rapidly and to a greater extent than inorganic forms (selenite and selenate). However, no significant difference in the response of both plasma and erythrocyte GSH-Px activity could be observed. In contrast, platelet GSH-Px activity was more sensitive to the chemical form of Se administered. Saturation of platelet GSH-Px activity occurred at lower plasma Se levels when selenite or selenate were used as Se supplements than with the organic forms. Interpretation of some of the results is provided and ideas are suggested for consideration in further studies.

Blood Platelets↗
PubMed2002

Use of phenyl 2-alpha-selenoglycosides of N-acetylneuraminic acid as a glycosyl donor for the glycosylation reactions.

Phenyl 2-alpha-selenoglycosides of Neu5Ac were successfully prepared from the corresponding peracetylated chloro derivative of Neu5Ac 1 and phenylselenol in the presence of N,N-di-isopropylethylamine in excellent yields. The reaction of with various alcohols was effectively catalyzed by NIS/TfOH or DMTST to produce a variety of glycosides in moderate yields. Selective activation of over phenyl 2-alpha-thioglycoside of Neu5Ac with AgOTf/K(2)CO(3) was also achieved.

Glycosides↗
PubMed1993

Bioactivity and molecular modelling of diphenylsulfides and diphenylselenides.

Bis(2-bromo-4,5-dimethoxyphenyl)sulfide (5) and bis(2-bromo-4,5-dimethoxyphenyl) selenide (7) have been shown to block cells in the G2/M phase of the cell cycle, whereas the debromo (4,6) equivalents do not. The biobromoselenide (7) is cytotoxic to tumour cells in vitro and has been shown to increase the mitotic index of treated cells. These biological effects are consistent with disruption of the mitotic apparatus. This agent does not inhibit microtubule assembly in vitro, but does bind to tubulin. Molecular modelling of these structures indicates that their spatial and electronic structures may make an important contribution to the biological activity.

Animals↗
PubMed2000

Selenate-supplemented nutritional formula increases plasma selenium in hemodialysis patients.

OBJECTIVE: The purpose of this study was to determine the short-term effect of feeding selenium-supplemented formulas on the selenium status of end-stage renal disease patients on hemodialysis. DESIGN AND SETTING: The prospective, randomized, single-blind study of parallel design was conducted at three hemodialysis clinics. PATIENTS: A total of 79 hemodialysis patients were randomly assigned into one of three groups. INTERVENTION: Liquid nutritional formula supplemented with either selenite (28 microg Se/8 oz, n = 26), selenate (28 microg Se/8 oz, n = 26), or nonfortified (7 microg Se/8 oz, n = 27) was fed to hemodialysis patients as their sole source of nutrition for 14 days. MAIN OUTCOME MEASURE: Plasma and red blood cell (RBC) selenium and glutathione peroxidase (GPX) activities were measured in predialysis blood both before (day 1) and after (day 8) a 7-day baseline period, and after subjects received the formula as the sole source of nutrition (approximately 35 kcal/kg/d) for 14 days (day 22). RESULTS: Selenium intake (Mean +/- SEM, microg/d) was 134 +/- 9, 140 +/- 9, and 35 +/- 2 for patients receiving selenite-, selenate-, or non-supplemented formula, respectively. On day 22, plasma selenium (micromol/L) was greater (P <.032) in the selenate-supplemented group (1.5 +/- 0.1) compared with the nonsupplemented group (1.2 +/- 0.1), but not compared with the selenite-supplemented group (1.4 +/- 0.1). Plasma GPX activity was 44% to 60% that of healthy controls and not different among groups. RBC selenium and GPX activities were within the normal range and were not different among groups. CONCLUSION: The results of this study indicate that a liquid formula supplemented with selenium as selenate is successful at maintaining selenium concentrations within normal range, as well as significantly increasing plasma selenium levels compared with nonsupplementation.

Adult↗
PubMed2003

Influence of selenium sources on age-related and mild heat stress-related changes of blood and liver glutathione redox cycle in broiler chickens (Gallus domesticus).

Selenium is an essential trace element that up-regulates a major component of the antioxidant defense mechanism by controlling the body's glutathione (GSH) pool and its major Se-containing antioxidant enzyme, glutathione peroxidase (GPX). Evidence has emerged suggesting that organic selenium, natural seleno-amino acids found in plants, grains and selenized yeast, maintains the antioxidant defense system more efficiently than inorganic selenium. Inorganic selenium is a pro-oxidant, whereas organic selenium possesses antioxidant properties itself. As a pro-oxidant, inorganic selenium is not suitable for animals or humans. Therefore, we examined the GSH-GPX system in broiler chickens and determined that organic selenium was indeed more beneficial than inorganic selenium. Chickens fed the organic selenium as Sel-Plex, a selenized yeast, had elevated GPX activity in both blood and liver in a thermoneutral environment and after heat distress. More importantly, the ability to reduce the oxidized glutathione (GSSG to 2 GSH) was enhanced and facilitated by maintenance of glutathione reductase activity. Organic selenium-fed chickens were less affected by mild heat distress than inorganic selenium-fed chickens, and this assessment was based upon less induction of heat shock protein 70 (hsp70) in organic selenium-fed chickens. Our results clearly show that heat distress, a potent inducer of oxidative stress and hsp70, can be partially ameliorated by feeding organic selenium. We attribute this observation to an enhanced GSH-GPX antioxidant system in organic selenium-fed chickens.

Aging↗
PubMedDate not supplied

Post firing visualisation of fingerprint on spent cartridge cases.

A considerable range of techniques is available to visualise latent fingerprints on smooth surfaces. Published methods and those developed or modified in the authors' laboratory have been evaluated for spent cartridge cases. The most suitable were found to be vacuum cyanoacrylate (with fluorescent staining) and selenious acid treatments. Both were used to investigate the post firing recovery of finger-marks on spent cartridge cases from the ammunition and weapon systems encountered in terrorist casework in Northern Ireland. Only certain revolvers and the SLR rifle yielded identifiable ridge detail. These results are borne out by casework experience.

Cyanoacrylates↗
PubMed1997

Selenium salts and chromosome damage.

Sodium selenite and sodium selenate, fed by gavaging to age-matched male Swiss albino mice and observed after 24 h following a colchicine-fixative-air drying-Giemsa schedule, were found to induce chromosome breaks and spindle disturbances in bone marrow cells. The four concentrations used were fractions of LD50 and the effects were directly proportionate to the concentration of the chemical. Sodium selenite induced a slightly higher frequency of chromosomal aberrations than sodium selenate.

Animals↗