			Home About us Contact

Diphenyl Diselenide (diphenyl + diselenide)

Distribution by Scientific Domains

Chemistry	77%
Medical Sciences	22%

Selected Abstracts

Diphenyl Diselenide and Ascorbic Acid Changes Deposition of Selenium and Ascorbic Acid in Liver and Brain of Mice

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2001
Maria Caroline Jacques-Silva
These compounds have been reported to inhibit the cerebral and hepatic aminolevulinic acid dehydratase (ALA-D) in vitro, and now we show that ascorbic acid can reverse some alterations caused by in vivo selenium exposure, but not ALA-D inhibition. The effect of Na2SeO3 or (PhSe)2 and ascorbic acid on selenium distribution, total non-protein thiol, ascorbic acid content (liver and brain) and haemoglobin was also examined. Mice were exposed to 250 ,mol/kg (PhSe)2, or 18.75 ,mol/kg Na2SeO3 subcutaneously, and to ascorbic acid, twice a day, 1 mmol/kg intraperitonially, for 10 days. Hepatic ALA-D of mice treated with (PhSe)2 was inhibited about 58% and similar results were observed in the animals that received ascorbic acid supplementation (P<0.01, for (PhSe)2 -treated and (PhSe)2+ascorbic acid-treated mice). The haemoglobin content decreased after treatment with (PhSe)2 (P<0.01). However, the haemoglobin content of the (PhSe)2+ascorbic acid group was significantly higher than in the (PhSe)2 -treated mice (P<0.05), and similar to control (P>0.10). Ascorbic acid treatment decreased significantly the hepatic and cerebral deposition of Se in (PhSe)2 -exposed mice (P<0.01). Hepatic non-protein thiol content was not changed by treatment with (PhSe)2, ascorbic acid or (PhSe)2+ascorbic acid. Hepatic content of ascorbic acid was twice that in mice that received (PhSe)2, independent of ascorbic acid treatment (P<0.001). The results of this study suggest that vitamin C may have a protective role in organodiselenide intoxication. [source]

ChemInform Abstract: Oxidation of Alkynes in Aqueous Media Catalyzed by Diphenyl Diselenide.

CHEMINFORM, Issue 39 2010
Stefano Santoro
Abstract An unprecedented transformation is discovered under conditions A). [source]

ChemInform Abstract: The Reaction of Mono-Aryl Substituted Methylenecyclobutanes with Diphenyl Diselenide in the Presence of Iodosobenzene Diacetate and H2O.

CHEMINFORM, Issue 22 2009
Min Jiang
Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

ChemInform Abstract: Hydrothiolation of Terminal Alkynes with Diaryl Disulfides and Diphenyl Diselenide: Selective Synthesis of (Z)-1-Alkenyl Sulfides and Selenides.

CHEMINFORM, Issue 12 2009
Zhang-Lin Wang
Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

Copper(II) Acetate Mediated Reactions of Methylenecyclopropane and Diphenyl Diselenide.

CHEMINFORM, Issue 42 2007
Lei Yu
Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF. [source]

Ring-Opening Reactions of Methylenecyclopropanes with Diphenyl Diselenide upon Heating; Formation of 3-Phenylselenyl-2,5-dihydrofuran Derivatives.

CHEMINFORM, Issue 18 2005
Le-Ping Liu
Abstract For Abstract see ChemInform Abstract in Full Text. [source]

ChemInform Abstract: Oxidation of Diphenyl Diselenide with 2,3-Dichloro-5,6-dicyanobenzoquinone (DDQ).

CHEMINFORM, Issue 10 2002
A New Method for the Electrophilic Phenylselenenylation of Alkenes under Mild Conditions.
Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

Diphenyl diselenide protects against glycerol-induced renal damage in rats

JOURNAL OF APPLIED TOXICOLOGY, Issue 7 2009
Ricardo Brandão
Abstract In this study we evaluated the effect of diphenyl diselenide (PhSe)2 on glycerol-induced acute renal failure in rats. Rats were pre-treated by gavage every day with (PhSe)2 (7.14 mg kg,1) for 7 days. On the eighth day, rats received an intramuscular injection of glycerol (8 mL kg,1). Twenty-four hours afterwards, rats were euthanized and the levels of urea and creatinine were measured in plasma. Catalase (CAT), glutathione peroxidase (GPx), glutathione S -transferase (GST), , -aminolevulinate dehydratase (, -ALA-D) and Na+, K+ -ATPase activities and ascorbic acid levels were evaluated in renal homogenates. Histopathological evaluations were also performed. The results demonstrated that (PhSe)2 was able to protect against the increase in urea and creatinine levels and histological alterations in kidney induced by glycerol. (PhSe)2 protected against the inhibition in , -ALA-D, CAT and GPx activities and the reduction in ascorbic acid levels induced by glycerol in kidneys of rats. In conclusion, the present results indicate that (PhSe)2 was effective in protecting against acute renal failure induced by glycerol. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in mice

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2008
Ricardo Brandão
Abstract Mercury is a heavy metal that can cause a variety of toxic effects on the organism, such as hematological and immunological alterations. In the present investigation, deleterious effects of mercury-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 were studied. Male adult Swiss albino mice received daily a pretreatment with (PhSe)2 (15.6 mg/kg, orally) for 1 week. After this week, mice received daily mercuric chloride (1 mg/kg, subcutaneously) for 2 weeks. A number of hematological (erythrocytes, leukocytes, platelets, hemoglobin, hematocrit, reticulocytes, and leukocytes differential) and immunological (immunoglobulin G and M plasma concentration) parameters were evaluated. Another biomarker of tissue damage, lactate dehydrogenase (LDH), was also determined. The results demonstrated that mercury exposure caused a reduction in the erythrocyte, hematocrit, hemoglobin, leukocyte, and platelet counts and an increase in the reticulocyte percentages. (PhSe)2 was effective in protecting against the reduction in hematocrit, hemoglobin, and leukocyte levels. (PhSe)2 ameliorated reticulocyte percentages increased by mercury. However, (PhSe)2 was partially effective in preventing against the decrease in erythrocyte and platelet counts. Immunoglobulin G and M concentrations and LDH activity were increased by mercury exposure, and (PhSe)2 was effective in protecting against these effects. In conclusion, (PhSe)2 was effective in protecting against hematological and immunological alterations induced by mercury in mice. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:311,319, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20242 [source]

Platinum Complexes of Aromatic Selenolates

EUROPEAN JOURNAL OF INORGANIC CHEMISTRY, Issue 25 2010
Amy L. Fuller
Abstract Several synthetic methods are used to prepare naphthalene-based aromatic 1,2-diselenoles. A new one-pot synthesis starting from naphthalene is used to produce theknown compound naphtho[1,8- c,d][1,2]diselenole (Se2naph).Friedel,Crafts alkylation is used on Se2naph to substitute either one tert -butyl group to form 2- tert -butylnaphtho[1,8- c,d][1,2]diselenole (mt-Se2naph) or two tert -butyl groups to form 2,7-di- tert -butylnaphtho[1,8- c,d][1,2]diselenole (dt-Se2naph). Bromination of mt-Se2naph results in dibromination of the naphthalene ring, rather than reaction at selenium, to give 4,7-dibromo-2- tert -butylnaphtho[1,8- c,d][1,2]diselenole (mt-Se2naphBr2). Reduction of the Se,Se bond in Se2naph, mt-Se2naph, dibenzo[c,e][1,2]diselenine (dibenzSe2), or diphenyl diselenide (Se2Ph2) with LiBEt3 H, followed by in-situ addition of [PtCl2{P(OPh)3}2] yields the four-coordinate mono- and dinuclear platinum(II) bis(phosphite) complexes [Pt(Se2naph){P(OPh)3}2] (1), [Pt(mt-Se2naph){P(OPh)3}2] (2), [Pt2(dibenzSe2)2{P(OPh)3}2] (3), cis -[Pt(SePh)2{P(OPh)3}2] (4), and trans -[Pt2(SePh)4{P(OPh)3}2] (5). [source]

Lanthanum(III) Oxide as a Recyclable Catalyst for the Synthesis of Diaryl Sulfides and Diaryl Selenides

EUROPEAN JOURNAL OF ORGANIC CHEMISTRY, Issue 34 2009
Sabbavarapu Narayana Murthy
Abstract La2O3 as a new and efficient recyclable catalyst in coupling various aryl halides with aromatic/alkyl thiols and diphenyl diselenide in combination with KOH as a base and DMEDA as a ligand in DMSO at 110 °C is reported. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009) [source]

Diphenyl diselenide protects against glycerol-induced renal damage in rats

Oral administration of diphenyl diselenide potentiates hepatotoxicity induced by carbon tetrachloride in rats

JOURNAL OF APPLIED TOXICOLOGY, Issue 2 2009
Cristina W. Nogueira
Abstract Carbon tetrachloride (CCl4) is a model for studying free radical-induced liver injury and screening hepato-protective drugs. Numerous studies have reported the involvement of oxidative stress in CCl4 -induced liver damage and the hepato-protective effects mediated by different antioxidants. The present study examined the effects of diphenyl diselenide, (PhSe)2, on hepatotoxicity induced by CCl4 in rats. To this end, male Wistar rats received (PhSe)2 by oral route at the dosage of 31.2 mg/kg for one or two days. After the second day of treatment, rats received CCl4 orally in a single dose. The liver and kidney were utilized for determination of histopathology, biochemical [aspartate (ALT) and alanine (AST) aminotransferases, alkaline phosphatase (ALP), total bilirrubin (TB) and gamaglutamyl transferase (GGT)] and toxicological parameters [thiobarbituric reactive species (TBARS) levels, catalase activity, ascorbic acid, nonprotein thiols (NPSH) and aminolevulinate dehydratase (, -ALA-D) activity]. Repeated administration of (PhSe)2 caused a marked potentiation of hepatotoxicity induced by CCl4 exposure, as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of TBARS levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid. Pre-treatment with a single dose of (PhSe)2 prevented the effect of strychnine, a substrate for CYPs, abolishing lethality in mice. This result indicates that (PhSe)2 prevented animal death, suggesting an activator action of (PhSe)2 in CYPs. This study clearly indicates that (PhSe)2 potentiated acute hepatic damage induced by CCl4. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in mice

Voltage-dependent ebselen and diorganochalcogenides inhibition of 45Ca2+ influx into brain synaptosomes

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2003
M. B. Moretto
Abstract By mediating the Ca2+ influx, Ca2+ channels play a central role in neurotransmission. Chemical agents that potentially interfere with Ca2+ homeostasis are potential toxic agents. In the present investigation, changes in Ca2+ influx into synaptosomes by organic forms of selenium and tellurium were examined under nondepolarizing and depolarizing conditions induced by high KCl concentration (135 mM) or by 4-aminopyridine (4-AP). Under nondepolarizing conditions, ebselen (400 ,M) increased Ca2+ influx; diphenyl ditelluride (40,400 ,M) decreased Ca2+ in all concentrations tested; and diphenyl diselenide decreased Ca2+ influx at 40 and 100 ,M, but had no effect at 400 ,M. In the presence of KCl as depolarizing agent, ebselen and diphenyl ditelluride decreased Ca2+ influx in a linear fashion. In contrast, diphenyl diselenide did not modify Ca2+ influx into isolated nerve terminals. In the presence of 4-AP (3 mM) as depolarizing agent, ebselen (400 ,M) caused a significant increase, whereas diphenyl diselenide and diphenyl ditelluride inhibited Ca2+ influx into synaptosomes. The results can be explained by the fact that the mechanism through which 4-AP and high K+ induced elevation of intracellular Ca2+ is not exactly coincident. The mechanism by which diphenyl ditelluride and ebselen interact with Ca2+ channel is unknown, but may be related to reactivity with critical sulfhydryl groups in the protein complex. The results of the present study indicate that the effects of organochalcogenides were rather complex depending on the condition and the depolarizing agent used. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:154,160, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10073 [source]

Bis-(3-hydroxyphenyl) diselenide inhibits LPS-stimulated iNOS and COX-2 expression in RAW 264.7 macrophage cells through the NF- kB inactivation

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2009
Kyung-Min Shin
Abstract Objectives Previously, we reported that diaryl diselenide compounds have strong inhibitory effects on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in macrophages. In this study, we investigated the molecular mechanisms underlying NO suppression and prostaglandin E2 (PGE2) production by diaryl diselenide compounds, bis-(2-hydroxyphenyl) diselenide (DSE-A), bis-(3-hydroxyphenyl) diselenide (DSE-B), bis-(4-hydroxyphenyl) diselenide (DSE-C), dipyridyl diselenide (DSE-D) and diphenyl diselenide (DSE-E). Methods The effect of these compounds on NO suppression and PGE2 production was investigated in RAW 264.7 macrophages. Key findings Our data indicate that of the above, DSE-B most potently inhibits NO and PGE2 production, and that it also significantly reduces the releases of tumour necrosis factor (TNF)-,, interleukin(IL)-1, and IL-6. Consistent with these observations, DSE-B also reduced the protein levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), and the mRNA levels of iNOS, COX-2, TNF-,, IL-1, and IL-6. Furthermore, DSE-B inhibited LPS-induced nuclear factor-,B (NF-,B) activation, which was associated with the prevention of the inhibitor ,B-, (I,B-,) degradation and a subsequent reduction in nuclear p65 protein levels. Conclusions Taken together, our data suggest that the anti-inflammatory properties of DSE-B are due to reduction in the expression of iNOS, COX-2, TNF-,, IL-1, and IL-6 through the down-regulation of NF-,B binding activity. [source]

Mechanisms involved in the antinociceptive effect caused by diphenyl diselenide in the formalin test

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 12 2008
Lucielli Savegnago
This study investigated the mechanisms involved in the antinociceptive action induced by diphenyl diselenide ((PhSe)2) in the formalin test. Mice were pre-treated with (PhSe)2 by the oral route (0.1,100 mg kg,1), 30 min before formalin injection. To address some of the mechanisms by which (PhSe)2 inhibits formalin-induced nociception mice were treated with different drugs. The antinociceptive effect of (PhSe)2 was shown in the first and second phases of the formalin test. The antinociceptive effect caused by (PhSe)2 (10 mg kg,1, p.o.) was prevented by intrathecal injection of K+ channel blockers such as apamin and charybdotoxin (small- and large-conductance Ca2+ -activated K+ channel inhibitors, respectively) and tetraethylammonium (TEA, a non-selective voltage-dependent K+ channel inhibitor), but not glib-enclamide (an ATP-sensitive K+ channel inhibitor). The antinociceptive action caused by (PhSe)2 (10 mg kg,1, p.o.) was also blocked by a nitric oxide (NO) synthase inhibitor (N, -nitro- l -arginine, L-NOARG) and the soluble guanylate cyclase inhibitors 1H -[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ) and methylene blue. These results suggest the participation of NO/cyclic GMP/Ca2+ and K+ channel pathways in the antinociceptive effect caused by (PhSe)2. [source]