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PubMed2000

Increase in dopamine metabolites in murine striatum after oral exposure to inorganic but not organic form of selenium.

Selenium (Se) is an essential as well as a toxic trace element. Se intoxication has been reported in both livestock and humans. The central nervous system is sensitive to Se poisoning; exposure to Se causes blind staggers in cattle, poliomyelomalacia in pigs, and nervous system disorders in humans. Differences in neurotoxicity between inorganic and organic Se have been demonstrated. In this study, groups of five male BALB/c mice each were administered sodium selenite or selenomethionine in drinking water ad libitum at 0, 1, 3, and 9 ppm as Se for 14 days. At the end of Se exposure, their brains were removed and dissected into different regions. The concentration of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindolacetic acid (5-HIAA) were determined in each brain region. Food and water consumption and body weight gain were significantly decreased in the group treated with the highest concentration of sodium selenite. In mice administered sodium selenite at 3 and 9 ppm, DOPAC was significantly higher in the striatum than in the control group. The striatal HVA was also increased in the group treated with 3 ppm Se; the DA showed a similar pattern, but the increase was not statistically significant. No alterations of NE, 5-HT, or 5-HIAA levels were detected in any brain region of mice treated with sodium selenite. No significant differences in any parameter among the groups treated with selenomethionine were observed indicating that inorganic Se was more neurotoxic than organic Se via drinking water. The alterations of DA metabolites by inorganic Se in DA-rich striatum suggested a Se-specific increased neural activity of dopaminergic pathways. Results may be useful in further elucidation of neurotoxicity of Se and in establishing a safe level of intake for this element.

Administration, Oral↗
PubMed2006

Effect of selenium supplementation and source on the selenium status of horses.

This study was conducted to determine the effect of Se supplementation and source on the Se status of horses. Eighteen 18-mo-old nonexercised horses were randomly assigned within sex to 1 of 3 treatments: 1) control (CTRL, no supplemental Se, 0.15 mg of Se/kg of total diet DM); 2) inorganic Se (INORG, CTRL + 0.45 mg of Se/kg of total diet DM from NaSeO3); or organic Se [ORG, CTRL + 0.45 mg of Se/kg of total diet DM from zinc-L-selenomethionine (Availa Se, Zinpro, Corp., Eden Prairie, MN)]. Horses were acclimated to the CTRL diet (7.1 kg of DM alfalfa hay and 1.2 kg of DM concentrate per horse daily) for 28 d. After the acclimation period, the appropriate treatment was top-dressed on the individually fed concentrate for 56 d. Jugular venous blood samples were collected on d 0, 28, and 56. Middle gluteal muscle biopsies were collected on d 0 and 56. Muscle and plasma were analyzed for Se concentrations. Glutathione peroxidase activity was measured in muscle (M GPx-1), plasma (P GPx-3), and red blood cells (RBC GPx-1). Data were analyzed as a repeated measures design. Mean plasma Se concentration on d 28 and 56 was greater (P < 0.05) for Se-supplemented horses compared with CTRL horses, and tended (P < 0.1) to be greater in ORG vs. INORG on d 28. Mean muscle Se concentration and P GPx-3 activities increased (P < 0.05) from d 0 to 56 but were not affected by treatment. Mean RBC GPx-1 activity tended to be greater (P < 0.1) in ORG than INORG or CTRL horses on d 28, and tended to be greater (P < 0.1) for INORG compared with ORG horses on d 56. Mean RBC GPx-1 activity of INORG and ORG horses was not different from that of CTRL on d 56. Mean M GPx-1 activity decreased (P < 0.01) from d 0 to 56. In conclusion, zinc-L-selenomethionine was more effective than NaSeO3 at increasing plasma Se concentration from d 0 to 28; however, both supplemental Se sources had a similar effect by d 56. No difference in Se status due to Se supplementation or source could be detected over a 56-d supplementation period by monitoring middle gluteal muscle Se, M GPx-1, or P GPx-3. Results for RBC GPx-1 also were inconclusive relative to the effect of Se supplementation and source.

Animal Feed↗
PubMed2001

The selenoorganic compound ebselen suppresses liver injury induced by Propionibacterium acnes and lipopolysaccharide in rats.

Ebselen (2-phenyl-1,2-benzoisoselenazol-3[2H]-one) is a selenoorganic compound containing selenium that has various pharmacological effects, including anti-inflammatory and antioxidant activity. Kupffer cells, residual hepatic macrophages, play an important role in the development of liver injury by producing free radicals and cytokines. The aim of this study is to evaluate whether ebselen suppresses macrophage-associated liver injury in rats. In vivo, we examined the effects of ebselen on liver injury, induced by Propionibacterium acnes and lipopolysaccharide (P. acnes-LPS), in rats where hepatic macrophages are considered to be primarily involved in injury development. Ebselen administration reduced the incidence of death following hepatic failure by P. acnes-LPS (82% vs. 20%, p<0.05). Serum levels of alanine aminotransferase, at 5 h after LPS administration, were significantly lower in the ebselen-treated group than in the control group (202.4+/-100.3 IU/l vs. 558.4+/-146.4 IU/l, p<0.05). Histological evidence of injury, such as necrosis, hemorrhage, and degeneration, was also suppressed by ebselen. Further, to assess the mechanisms involved, we investigated the production of cytokines and superoxide anions produced by activated hepatic macrophages in vivo. Serum levels of TNF alpha, interleukin-18 (IL-18)/IFN gamma-inducing factor (IGIF), and interferon gamma (IFN gamma) at 1 h after LPS administration were significantly lower in the ebselen-treated group. Formazan depositions, which were generated by the perfusion of the liver with nitroblue tetrazolium, were also observed less frequently in the ebselen treated group, suggesting a suppression in the release of superoxide anion from activated hepatic macrophages. In addition, we examined the effects of ebselen on cytokine production and mRNA expression, in vitro, using rat primary Kupffer cell culture. Ebselen also inhibited TNF alpha production and mRNA expression in vitro. These data imply that ebselen suppresses liver injury by inhibiting the production and/or release of proinflammatory cytokines and superoxide from activated hepatic macrophages. These data also suggest that ebselen is potent in the prevention of hepatic injury, such as endotoxemia, where hepatic macrophage activation has been implicated.

Alanine Transaminase↗
PubMed2003

Modulation of the arsenic effects on cytotoxicity, viability, and cell cycle in porcine endothelial cells by selenium.

The differential effects of arsenic compounds and the effect of selenium on arsenic-induced changes in cytotoxicity, viability, and cell cycle of porcine aorta endothelial cells (PAECs) were investigated. MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay indicated that arsenic trioxide (As(2)O(3)) and sodium arsenite (NaAsO(2)) showed similar cytotoxicity, whereas sodium arsenate (Na(2)HAsO(4)) did not show cytotoxicity in PAECs. As(2)O(3) and NaAsO(2) at 20 microM decreased PAEC viability, decreased G0/G1 phase, and increased apoptosis. An increased G2/M phase was observed in NaAsO(2)-treated PAECs, whereas an increase in secondary necrosis (late apoptosis) was observed in As(2)O(3)-treated PAECs. As(2)O(3)-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO(2)-induced apoptosis was associated with p53 upregulation. Sodium selenite (Na(2)SeO(3)) at 1 nM reduced 20 microM As(2)O(3)-induced cytotoxicity, but not apoptosis, at 24 h. Increased glutathione peroxidase (GPX) activity by Na(2)SeO(3) pretreatment in 20 microM As(2)O(3)-treated PAECs suggests that Na(2)SeO(3) modulates As(2)O(3)-induced cytoxicity by GPX modulation.

Animals↗
PubMed1995

Comparison of 1% and 2.5% selenium sulfide in the treatment of tinea capitis.

OBJECTIVE: To determine whether an over-the-counter shampoo containing 1% selenium sulfide would have sporicidal activity equal to that of a 2.5% selenium sulfide prescription lotion in the adjunctive treatment of tinea capitis infection. DESIGN: Prospective randomized nonblinded clinical trial. SETTING: Outpatient clinics and emergency department of a children's hospital. PATIENTS: Fifty-four patients between the ages of 1 and 15 years with culture-proved tinea capitis infection caused by Trichophyton tonsurans enrolled during a 14-month period. METHODS: Patients were randomized to receive 2.5% selenium sulfide lotion, 1% selenium sulfide shampoo, or a bland, nonmedicated shampoo with which they were instructed to shampoo twice weekly. All received 15 mg/kg per day of griseofulvin. Dermatophyte cultures of the affected area of each patient's scalp were obtained on enrollment and every 2 weeks until a negative culture was obtained from a previously infected area. RESULTS: Survival data analysis demonstrated that both the 2.5% selenium sulfide and 1% selenium sulfide preparations were superior to the nonmedicated control shampoo in terms of the time required to eliminate shedding of viable spores. When compared with each other, there was no difference between the 2.5% selenium sulfide and 1% selenium sulfide preparations in time required to produce a negative culture. CONCLUSION: Commercially available 1% selenium sulfide shampoo is an equally effective yet less expensive alternative sporicidal therapy in the adjunctive treatment of tinea capitis infection.

Adolescent↗
PubMed1998

Zinc-containing afferent projections to the rat corticomedial amygdaloid complex: a retrograde tracing study.

The mammalian amygdaloid complex is densely innervated by zinc-containing neurons. The distribution of the terminals throughout the region has been described, but the origins of these zinc-containing fibers have not. The present work describes the origins of one major component of the zinc-containing innervation of the amygdaloid complex, namely, the component that innervates the corticomedial complex. Selective labeling of zinc-containing axons was accomplished by intracerebral microinfusion of selenium anions (SeO3(2-)), a procedure that produces a ZnSe precipitate in zinc-containing axonal boutons with subsequent retrograde transport to the neurons of origin. After infusions of SeO3(2-) into combinations of cortical, medial, or amygdalohippocampal regions, retrogradely labeled zinc-containing somata were found in all amygdaloid nuclei except for the medial and central nuclei, the bed nucleus of the accessory olfactory tract, the nucleus of the lateral olfactory tract, and the anterior amygdaloid area. Extrinsic zinc-containing projections to the same amygdaloid terminal fields were found to originate from the infralimbic, cingulate, piriform, perirhinal and entorhinal cortices, and from the prosubiculum and CA1. Commissural zinc-containing projections were found to originate from the posterolateral and posteromedial cortical nuclei and from the posterior part of the basomedial nucleus. Zinc-containing neurons have been implicated in the pathophysiology of epilepsy, in cell death after seizure or stroke, and in Alzheimer's disease, all clinical conditions that involve the amygdaloid complex. Identification of the zinc-containing pathways is a prerequisite to the elucidation of zinc's role in these disorders.

Alzheimer Disease↗
PubMed1999

Effects of glutathione depletion on selenite- and selenate-induced embryotoxicity in cultured rat embryos.

Effects of depletion of reduced glutathione (GSH) on selenium (Se) embryotoxicity in cultured rat embryos were examined. Rat embryos at day 9.5 of gestation were cultured for 48 h in the presence of Se as either sodium selenite at 10 and 20 microM or sodium selenate at 30 and 100 microM. Embryonic GSH was depleted by the addition of 0.1 mM of L-buthionine-[S,R]-sulfoximine (BSO) without embryotoxicity, i.e., significant growth retardation and malformation of the embryos. Selenite at 10 microM or selenate at 100 microM significantly increased the incidence of malformation of the embryos. The incidence of selenite-induced malformation of the embryos at 20 microM was significantly decreased with BSO. On the contrary, the incidence of selenate-induced malformation at 30 microM was significantly increased with BSO. It was noted that the major malformed regions of the embryos by the embryotoxic concentration of BSO alone were the same to those affected by selenite or selenate. It was considered from these results that embryonic GSH was involved in the embryotoxicity of selenite and selenate. The embryotoxicity of selenate may not be mediated through the reduction to selenite. It was suggested that the formation of selenodiglutathione and the oxidative stress were involved in the embryotoxicity of selenite and selenate, respectively.

Animals↗
PubMedDate not supplied

A selenide linker for "traceless" solid-phase organic synthesis.

4-Bromophenethyl alcohol was protected as the THP ether, followed by reaction with magnesium and selenium to give the corresponding diselenide. Ether deprotection provides a diselenide diol, which is attached to solid-phase resins. The polymer-bound selenide anion is then generated, and functions as a traceless linker for electrophiles such as alkyl halides.

Organic Chemicals↗
PubMed2002

An organometallic route to oligonucleotides containing phosphoroselenoate.

Unlike the widespread use of phosphorothioates in nucleic acid chemistry, complementary research on phosphoroselenoates has been severely limited. Previous routes to DNA and RNA that contain phosphoroselenoates employ elemental Se and KSeCN as Se transfer agents, although these reagents suffer from low or unselective reactivity. The metastability of the Pbond;Se bond demands soluble, selective Se transfer reagents. The organometallic reagent (iPrC(5)H(4))(2)TiSe(5) satisfies these criteria, as we demonstrate by the synthesis of phosphoroselenoate derivatives of mono- and oligonucleotides of DNA and a dinucleotide of RNA. The new general method is compatible with high-throughput phosphoramidate oligonucleotide synthesis, which allows for the preparation of site-specifically labeled oligonucleotides. A (31)P NMR spectroscopy study shows that the phosphoroselenoate of (5')-d(GGAATGTC(Se)TGTCG)-(3') selectively binds to soft Cd(2+) ions but not Mg(2+) ions.

Cations, Divalent↗