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21.
Ayaz M Ozdemir S Ugur M Vassort G Turan B 《Archives of biochemistry and biophysics》2004,426(1):83-90
Since selenium compounds can restore some metabolic parameters and structural alterations of diabetic rat heart, we were tempted to investigate whether these beneficial effects extend to the diabetic rat cardiac dysfunctions. Diabetes was induced by streptozotocin (50mg/kg body weight) and rats were then treated with sodium selenite (5 micromol/kg body weight/day) for four weeks. Electrically stimulated isometric contraction and intracellular action potential in isolated papillary muscle strips and transient (I(to)) and steady state (I(ss)) outward K(+) currents in isolated cardiomyocytes were recorded. Sodium selenite treatment could reverse the prolongation in both action potential duration and twitch duration of the diabetic rats, and also cause significant increases in the diminished amplitudes of the two K(+) currents. Treatment of rats with sodium selenite also markedly increased the depressed acid-soluble sulfhydryl levels of the hearts. Our data suggest that the beneficial effects of sodium selenite treatment on the mechanical and electrical activities of the diabetic rat heart appear to be due to the restoration of the diminished K(+) currents, partially, related to the restoration of the cell glutathione redox cycle. 相似文献
22.
M. A. Amoozegar J. Hamedi M. Dadashipour S. Shariatpanahi 《World journal of microbiology & biotechnology》2005,21(6-7):1237-1243
Summary Ten moderately halophilic spore-forming bacilli were isolated from saline soils in Iran and their intrinsic high-level resistance
to chromate, arsenate, tellurite, selenite, selenate and biselenite was identified by an agar dilution method. Minimum inhibitory
concentration (MIC) for each oxyanion was determined. All isolates were resistant to higher concentrations of arsenate. The
resistance level of the isolates to selenooxyanions was between 10 and 40 mM. Maximum and minimum tolerance against oxyanions
was seen in selenite and biselenite, respectively. Although toxic metal resistance in the isolates was not different from
non-halophilic bacteria that has been reported, unusual resistance to arsenate (250 mM), sodium chromate (75 mM) and potassium
chromate (70 mM) was observed. The results obtained in this study revealed that all isolates were obviously susceptible to
silver, nickel, zinc and cobalt, while seven isolates were resistant to lead. Susceptibility to copper and cadmium varied
among the isolates. Silver had the maximum toxicity, whereas lead and copper showed minimum toxicity. The impact of salinity
on the toxicity of oxyanions was also studied. Our results showed that in general an increase in salinity from 5% (w/v) to
15% (w/v) enhanced tolerance to toxic oxyanions. 相似文献
23.
Mayumi Sato Tatsuo Nunoshiba Hajime Nishioka Takashi Yagi Hiraku Takebe 《Mutation research》1991,250(1-2):73-77
Sodium selenite was found to protect Escherichia coli cells against killing and mutagenic effects of N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Such protective effects were not observed when cells were treated with N-methyl-N-nitrosourea (MNU). The protection by sodium selenite was not controlled by the ada gene, which is responsible for the repair of alkylated damage in DNA. A reduction of the amount of glutathione was found when cells were treated with sodium selenite, and glutathione is known to be involved in the methylation of DNA by MNNG, not by MNU. Reduced methylation by MNNG due to the reduction of the amount of glutathione caused by abundant sodium selenite was suggested to be the mechanism of protection. 相似文献
24.
M. P. Arvy 《Plant and Soil》1989,117(1):129-133
Three hours after the absorption of selenite by the roots ofPhaseolus vulgaris a major part of the Se accumulates in the roots while the fraction conveyed towards the aerial organs is unevenly distributed. Uptake and distribution are enhanced when plants are kept in darkness or when the nutritive solution is supplied with glucose, suggesting an active transport of selenite. However, when roots are soaked in a low temperature solution or supplied with metabolic inhibitors, the level of Se decreased by about 35% in the roots and in the aerial organs. So, part of the selenite enters the roots by diffusion, while another part is metabolically linked. Sugar translocated from the leaves is implicated as a co-transport-substance for selenite. Antibiotics, such as gramicidin, synthetised by micro-organisms, can also increase the level of Se within the bean plant. 相似文献
25.
This study examined the use of vitamin E to alleviate toxic effects of sodium selenite. Adult male albino rats (n = 50) was divided into five groups. Group 1 was control, Groups 2 and 4 were treated with sodium selenite (2 mg/kg) for 2 and 4 weeks, respectively, Groups 3 and 5 were treated with sodium selenite (2 mg/kg) and vitamin E (100 mg/kg) for 2 and 4 weeks, respectively. Renal tissues were studied using anti-BCL2 and examined ultrastructurally. Positive Bax immunoreactivity was detected after 2 and more positive after 4 weeks and nearly all groups improved with co-administration of vitamin E. Ultrastructural study revealed lesions in Bowman's capsule and proximal convoluted tubules. The submicroscopic study revealed damage and necrosis of cortical structures after 2 and 4 weeks, respectively. After 4 weeks, cellular changes were seen, such as vacuolation and moderate degeneration of cells, widening of the urinary space scattered through the cortex with loss of cellular details, formation of apical buds, degeneration, and cellular rupture. Present findings disclosed an ameliorative effect of adding vitamin E to sodium selenite-induced changes in cortical tissues. Clinically, it is advised to add vitamin E to avoid selenium overdose hazards. 相似文献
26.
Nicholas V.C. Ralston Laura J. Raymond 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(11):2405-2416
Background
Methylmercury (CH3Hg+) toxicity is characterized by challenging conundrums: 1) “selenium (Se)-protective” effects, 2) undefined biochemical mechanism/s of toxicity, 3) brain-specific oxidative damage, 4) fetal vulnerability, and 5) its latency effect. The “protective effects of Se” against CH3Hg+ toxicity were first recognized >50?years ago, but awareness of Se's vital functions in the brain has transformed understanding of CH3Hg+ biochemical mechanisms. Mercury's affinity for Se is ~1 million times greater than its affinity for sulfur, revealing it as the primary target of CH3Hg+ toxicity.Scope of review
This focused review examined research literature regarding distinctive characteristics of CH3Hg+ toxicity to identify Se-dependent aspects of its biochemical mechanisms and effects.Conclusions
Research indicates that CH3Hg+ irreversibly inhibits the selenoenzymes that normally prevent/reverse oxidative damage in the brain. Unless supplemental Se is provided, consequences increase as CH3Hg+ approaches/exceeds equimolar stoichiometries with Se, thus forming HgSe and inducing a conditioned Se deficiency. As the biochemical target of CH3Hg+ toxicity, Se-physiology provides perspectives on the brain specificity of its oxidative damage, accentuated fetal vulnerability, and latency. This review reconsiders the concept that Se is a “tonic” that protects against CH3Hg+ toxicity and recognizes Se's role as Hg's molecular “target”. As the most potent intracellular nucleophile, the selenoenzyme inhibition paradigm has broad implications in toxicology, including resolution of conundrums of CH3Hg+ toxicity.General significance
Mercury-dependent sequestration of selenium and the irreversible inhibition of selenoenzymes, especially those required to prevent and reverse oxidative damage in the brain, are primarily responsible for the characteristic effects of mercury toxicity. 相似文献27.
Sonali Biswas Geeta Talukder Archana Sharma 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》1997,390(3):201
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. 相似文献
28.
Illuminated intact pea chloroplasts in the presence of O-acetylserine (OAS) catalysed incorporation of SeO32- and SO32- into selenocysteine and cysteine at rates of ca 0.36 and 6 μmol/mg Chl per hr respectively. Sonicated chloroplasts catalysed SeO32- and SO32- incorporation at ca 3.9 and 32% respectively of the rates of intact chloroplasts. Addition of GSH and NADPH increased the rates to ca 91 and 98% of the intact rates, but SeO32- incorporation under these conditions was essentially light-independent. In the absence of OAS, intact chloroplasts catalysed reduction of SO32- to S2- at rates of ca 5.8 μmol/mg Chl per hr. In the presence of OAS, S2- did not accumulate. Glutathione (GSH) reductase was purified from peas and was inhibited by ZnCl2. This enzyme, in the presence of purified clover cysteine synthase, OAS, GSH and NADPH, catalysed incorporation of SeO32- into selenocysteine (but not SO32- into cysteine). The reaction was inhibited by ZnCl2. Incorporation of SeO32- into selenocysteine by illuminated intact chloroplasts and sonicated chloroplasts (with NADPH and GSH) was also inhibited by ZnCl2 but not by KCN. Conversely, incorporation of SO32- into cysteine was inhibited by KCN but not by ZnCl2. It was concluded that SeO32- and SO32- are reduced in chloroplasts by independent light-requiring mechanisms. It is proposed that SeO32- is reduced by light-coupled GSH reductase and that the Se2- produced is incorporated into selenocysteine by cysteine synthase. 相似文献
29.
Tonin AA Da Silva AS Costa MM Otto MA Thomé GR Tavares KS Miletti LC Leal MR Lopes ST Mazzanti CM Monteiro SG de La Rue ML 《Experimental parasitology》2011,128(3):243-249
The aim of this study was to evaluate the utilization of a standard treatment with diminazene aceturate against the infection caused by Trypanosoma evansi, associated to sodium selenite and vitamin E. In vitro tests showed trypanocidal effect related to the treatment with diminazene aceturate and sodium selenite, but vitamin E had no harmful effect on the trypanosomes. In vivo experiments utilized a total of 72 adult outbreed females rats, separated into 9 groups (A, B, C, D, E, F, G, H and I), 8 animals each. Group A was the uninfected group; groups B to I were infected with 0.2 mL of blood containing 106 trypanosomes. Parasitemia was estimated daily by microscopic examination of blood smears. Group B served as positive control; group C was treated with diminazene aceturate; group D with sodium selenite; group E with vitamin E; group F received an association of diminazene aceturate and sodium selenite; group G received an association of diminazene aceturate and vitamin E; group H received an association of diminazene aceturate, sodium selenite and vitamin E, and group I received an association of sodium selenite and vitamin E. Diminazene aceturate was administrated in a single dose on the 3rd day post infection (PI). Sodium selenite and vitamin E were administered at the 3rd and 23rd day PI. In vivo tests showed increase of longevity in groups treated with diminazene aceturate associated with sodium selenite (groups F and H). No difference was found between groups C and E, thus the vitamin E did not increase the efficacy of treatment against T. evansi when associated to diminazene aceturate. The curative efficacy of treatments was 37.5, 87.7, 37.7 and 75% to the groups C, F, G and H, respectively. Other treatments showed no efficacy. The sodium selenite when combined with chemotherapy may represent an alternative in the treatment of trypanosomosis. 相似文献
30.
Inhibitor-of-apoptosis protein (IAP) inhibitors have been reported to synergistically reduce cell viability in combination with a variety of chemotherapeutic drugs via targeted cellular IAP (cIAP) depletion. Here, we found that cIAP silencing sensitised colorectal cancer (CRC) cells to selenite-induced apoptosis. Upon selenite treatment, the K63-linked ubiquitin chains on receptor-interacting protein 1 (RIP1) were removed, leading to the formation of the death-inducing complex and subsequent caspase-8 activation. Although the ubiquitinases cIAP1 and cIAP2 were significantly downregulated after a 24-h selenite treatment, cylindromatosis (CYLD) deubiquitinase protein levels were marginally upregulated. Chromatin immunoprecipitation assays revealed that lymphoid enhancer factor-1 (LEF1) dissociated from the CYLD promoter upon selenite treatment, thus abolishing suppression of CYLD gene expression. We corroborated these findings in a CRC xenograft animal model using immunohistochemistry. Collectively, our findings demonstrate that selenite caused CYLD upregulation via LEF1 and cIAP downregulation, both of which contribute to the degradation of ubiquitin chains on RIP1 and subsequent caspase-8 activation and apoptosis. Importantly, our results identify a LEF1-binding site in the CYLD promoter as a potential target for combinational therapy as an alternative to cIAPs. 相似文献