[Effect of sodium selenite, sodium tellurite and sodium sulfite on retention and distribution of mercury in mice].
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[Influence of sodium selenite, sodium tellurite and sodium sulfite on retention and distribution of cadmium in mice].
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Animals↗
[Level of cyclic AMP-dependent protein kinase isozyme in normal liver and hepatoma tissue and the effect of sodium selenite].
Sodium selenite in normal saline was administered intraperitoneally (1 mg/kg) into mice bearing ascitic hepatocarcinoma for 4 days. The cyclic AMP-dependent protein kinase isozymes (type I and type II) in normal liver and hepatocarcinoma cells were separated and assayed. The results show that the level of type I/II is markedly higher in hepatocarcinoma than in the normal liver cells. Sodium selenite is able to reduce it towards the normal level. Further analysis shows that the chief function of sodium selenite is to reduce the raised level of type I/II in hepatocarcinoma cells which, in fact, is due to the increase of total amount of type I cyclic AMP-dependent protein kinase. This paper presents the speculation that one of the mechanisms of the inhibitory effect of sodium selenite on carcinogenesis may be due to the selective action of this compound on the cyclic AMP-dependent protein kinase isozymes in tumor cells, thus inhibiting cancer cell division and facilitating differentiation and reversion.
Animals↗
Inhibition of zinc finger protein-DNA interactions by sodium selenite.
Sodium selenite and sodium selenate were analyzed for their ability to alter the DNA binding mechanisms of the Cys(2)His(2) zinc finger proteins, transcription factor IIIA (TFIIIA) and Sp1. TFIIIA is a positive regulator of 5S ribosomal RNA synthesis, and Sp1 is involved in cell proliferation and invasiveness. As assayed by DNase I protection, the interaction of the DNA binding domain of TFIIIA with the 5S ribosomal gene was inhibited by 25 microM selenite ions but not by 250 microM selenate ions. Selenite inhibition kinetics of TFIIIA progressed to completion in about 5 min. Preincubation of free TFIIIA with selenite resulted in DNA binding inhibition, whereas preincubation of a TFIIIA/5S RNA complex with selenite did not. Since 5S RNA binds to the TFIIIA DNA binding domain, this result is consistent with an inhibition mechanism via selenite binding to that region of this protein. Inhibition was not readily reversible and occurred in the presence of an excess of beta-mercaptoethanol; elevated amounts of dithiothreitol mitigated the inhibitory effect. Significantly less selenite (2.5-5 microM) inhibited the specific DNA binding of transcription factor Sp1 to the simian virus 40 (SV40) early promoter/enhancer. The selenite inhibition kinetics of Sp1 were fast, going to completion in about 1 min. SV40 DNA binding by the non-zinc finger transcription factor AP-2 was not inhibited by selenite. Inhibition of Cys(2)His(2) zinc finger proteins by micromolar amounts of selenite points to additional mechanisms for selenite-induced diminution of cell growth and anticancer activity.
Animals↗
Effect of dietary co-administration of sodium selenite on sodium arsenite-induced ovarian and uterine disorders in mature albino rats.
The subchronic treatment of mature female Wistar-strain albino rats in diestrous phase with sodium arsenite at a dose of 0.4 ppm/100 g body weight/rat/day via drinking water for period of 28 days (seven estrous cycles) caused a significant reduction in the plasma levels of leutinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol along with a significant decrease in ovarian activities of delta five, 3 beta-hydroxysteroid dehydrogenase (Delta5,3beta-HSD), and 17 beta-hydroxysteroid dehydrogenase (17beta-HSD) followed by a reduction in ovarian and uterine peroxidase activities. A significant weight loss of the ovary and uterus was also observed after this treatment, along with a prolonged diestrous phase and a high accumulation of arsenic in the plasma and these organs. Moreover, sodium arsenite was also responsible for ovarian follicular and uterine cell degeneration characterized by a high number of regressing follicles and a reduction in the uterine luminal diameter, respectively, in comparison with the controls. A dietary supplementation of sodium selenite at the dose of 0.6 mg/100 g body weight/rat/day for a period of 28 days along with arsenic treatment minimized the gonadal weight loss significantly and increased the activities of the ovarian steroidogenic enzymes as well as the ovarian and uterine peroxidase at the control level. Selenium was also able to increase the plasma levels of LH, FSH, and estradiol toward the control level. Vaginal smears showed normal estrous cyclicity in sodium selenite-supplemented arsenic-treated rats along with lower arsenic levels in the plasma and gonadal tissue in comparison with arsenic-only-treated rats. Histological sections of ovary and uterine tissues in the control and experimental groups confirmed that sodium selenite supplementation was able to prevent arsenic-induced histopathological changes in the ovary and uterus. Plasma levels of norepinephrine and dopamine in the midbrain and diencephalon decreased significantly, whereas the serotonin level was increased significantly after 28 days of sodium arsenite treatment. All of these parameters were, in most cases, unchanged from the control level when sodium selenite was co-administered with sodium arsenite. Arsenic intoxication was also associated with increased liver weight and elevation in the activities of hepatic and renal acid phosphatase, alkaline phosphatase, and transaminases, but selenium co-administration was not able to change these toxic effects of arsenic. The results of our experiments indicate the significant protective action of sodium selenite on arsenic-induced toxicity in the female reproductive system, while there was no significant protective effect of selenium on arsenic-induced toxicity in other organs.
Administration, Oral↗
Porcine focal symmetrical poliomyelomalacia: experimental reproduction with oral doses of encapsulated sodium selenite.
Sodium selenite (encapsulated as doses of 1.4 mg, 2.6 mg and 4.2 mg per kilogram of body weight) was given orally on a daily basis to male weaner pigs, and features of these animals were compared to a control group. Porcine focal symmetrical poliomyelomalacia was produced in all experimental groups between 3 and 20 days after initiation of the treatment. Analysis of blood and several tissues revealed an elevated selenium content for all pigs. Histological lesions in the brain and the cervical lumbar/sacral spinal cord enlargements included endothelial proliferation, neuronal degeneration, microcavitation and glial cell reaction.
Administration, Oral↗
[Glutathione peroxidase and glutathione reductase activity in the rat liver after the administration of sodium selenite].
Sodium selenite 24h after its single administration to rats causes an increase in the activity of glutathione peroxidase and glutathione reductase in the liver tissue. 6 h after the selenium administration the enzymes activity does not differ from the control. Doses of 0.15, 0.3, 0.5 and 1 mg of selenium per 1 kg of the animal weight were investigated. 0.3 mg proved to be the least effective dose. An increase in the enzyme activity after administering 0.5 mg of selenium is retained for 6 days and 14 days after it does not differ from the control. The liver relative weight 24 h after administration of 0.5 mg of selenium per 1 kg of animal weight proved to be higher but three days later it did not differ from the control. After administering selenium in a dose of 1 mg/kg the liver relative weight was higher for 6 days. Actinomycin D administered in a dose of 0.5 mg/kg simultaneously with selenite prevents the rise in the enzyme activity and relative weight of the liver caused only by a single injection of selenium in the same dose.
Animals↗
[Radioprotection of human endothelial cells by sodium selenite].
BACKGROUND: Sodium selenite is applied in tumor patients during chemo- or radiotherapy due to its cytoprotective effects. Aim of our study was to evaluate the effect of exposure with sodium selenite on proliferation of human endothelial and tumor cells after irradiation. MATERIALS AND METHODS: We studied the proliferative activity of human umbilical vein endothelial cells in comparison to tumor cells of the HeLa, MIA Paca-2 and SiHa cell line after single-dose irradiation with 2 or 10 Gy and controls without irradiation. All cells had been exposed to different concentrations of sodium selenite prior to irradiation. Evaluation was done by BrdU-ELISA. RESULTS: Exposure of human endothelial cells with sodium selenite concentrations > or = 100 micrograms/l led to an increase of BrdU proliferation index. This effect was markedly weaker in HeLa cells and not found in SiHa and MIA Paca-2. CONCLUSIONS: High concentrations of sodium selenite can counteract the decrease of proliferative activity caused by irradiation in human endothelial cells and thus exert a radioprotective effect on these cells. This effect was observed by far stronger in endothelial cells than in tumor cells, implying the possible clinical use of sodium selenite as a protective agent for normal tissue in radiotherapy.
Cell Division↗
[Efficacy of using combinations of sodium selenite and sodium nucleinate in the treatment of experimental myocardial infarct in the rabbit].
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Animals↗
Interaction of alkylmercuric compounds with sodium selenite. I. Metabolism of ethylmercuric chloride administered alone and in combination with sodium selenite in rats.
The effect of sodium selenite administered intragastrically in repeated doses to rats receiving ethylmercuric chloride po in various repeated doses (0.25 or 2.5 mg Hg/kg) on the excretion, whole-body retention, and organ distribution of mercury was studied. Selenium was found to affect the distribution of ethylmercury among tissues and subcellular fractions of the kidneys and liver as well as its binding to proteins of soluble fractions in these organs. Similarities and differences between the effect of interaction of sodium selenite with ethylmercuric chloride and methylmercury as well as inorganic mercury are also discussed.
Animals↗
Interaction of alkylmercuric compounds with sodium selenite. II. Metabolism of methylmercuric chloride administered alone and in combination with sodium selenite in rats.
Repeated doses of sodium selenite (Se) were administered to rats receiving repeated (IV or PO) doses of 0.25 or 2.5 mg Hg/kg methylmercuric chloride (Me2(203)Hg). Se (0.5 mg/kg) was observed to alter the distribution of Me203Hg among tissues as well as among subcellular fractions of kidneys and liver. An excess of selenium resulted in a twofold decrease in the mercury content of kidneys and a similar increase in the mercury content of brain.
Animals↗
Efficacy of dietary sodium selenite and calcium selenite provided in the diet at approved, marginally toxic, and toxic levels to growing swine.
A 2 x 3 factorial experiment conducted in three replicates of a randomized complete block design compared the effects of calcium selenite and sodium selenite at three different levels of Se (.3, 5, or 15 ppm) in the diets of growing swine on performance and tissue Se concentrations. Ninety pigs averaging 12.5 kg of BW were given ad libitum access to corn-soybean meal diets fortified with one of the treatment Se sources and dietary levels for a 35-d experimental period. Growth and feed intake were similar in pigs fed .3 and 5 ppm of Se but were lower (P less than .01) in those fed 15 ppm from either Se source. Serum Se increased (P less than .01) as dietary Se level increased with no difference between Se sources at each dietary Se level. Liver, kidney, and longissimus muscle Se concentrations increased (P less than .01) as the dietary level of Se increased and were similar when either Se sources was provided. These results indicate that calcium selenite was as effective as sodium selenite using the measurement criteria of growth, serum, and tissue Se concentrations and glutathione peroxidase activities of growing swine when fed at approved, marginally toxic, and toxic dietary Se levels.
Animal Feed↗
Interaction of alkylmercuric compounds with sodium selenite. III. Biotransformation, levels of metallothioneinlike proteins and endogenous copper in some tissues of rats exposed to methyl or ethylmercuric chloride with and without sodium selenite.
The biotransformation efficiency of alkylmercurial compounds was studied in rat liver, kidneys, blood, and brain after 2-week administration of methylmercuric chloride (MeHg) and ethylmercuric chloride (EtHg) at doses of 0.25 or 2.5 mg Hg/kg, alone or in combination with sodium selenite (Se) at a level of 0.5 mg Se/kg. Simultaneously, the level of metallothioneinlike proteins (MTP) and endogenous copper (Cu) was monitored in tissues of control rats and intoxicated rats. Regardless of the dose, the highest concentrations of inorganic mercury from both the alkylmercurials was found in the rat kidneys. Sodium selenite had a variable effect on the amount of inorganic mercury liberated, depending on the organ and the molar ratio of Hg:Se administered. A statistically significant increase in the levels of MTP and endogenous Cu, compared with control group, was found only in the kidneys of intoxicated rats. This increase was dependent on the concentration of inorganic mercury liberated by biotransformation of alkylmercurials. The observed changes appeared when the level of inorganic mercury exceeded 10 micrograms Hg/g tissue and reached a plateau at about 40 micrograms Hg/g tissue. In the presence of selenium the plateau of MTP and Cu levels were no observed in the kidneys, regardless of the amount of inorganic mercury liberated.
Animals↗
Activity of chosen indicator enzymes in blood serum of guinea pigs exposed to ethyl- and phenylmercuric chloride alone or jointly with sodium selenite.
The effect of sodium selenite on the activity of the selected enzymes in blood serum and on mercury concentration in some tissues of guinea pigs exposed to ethyl- (EtHg) or phenylmercuric chloride (PhHg) was investigated. Every second day for a 3-month period animals were given intragastrically a solution of mercuric compounds (2.5 mg Hg/kg) with or without sodium selenite (1 mg Se/kg). The activity of malate dehydrogenase (MDH, EC 1.1.1.37), phosphohexoizomerase (PHI, EC 5.3.1.9), and gamma-glutamyltranspeptidase (GGTP, EC 2.3.2.2) in blood serum of control animals was ca. 3.8, 325, and 48 IU. After 10 weeks of exposure to EtHg and PhHg, the activities (IU) of the above enzymes were, respectively, 5.9 and 6.5 (MDH), 585 and 600 (PHI) and 211 and 86.5 (GGTP). Sodium selenite administered with mercuric compounds did not prevent in increases in enzyme activity. During the experiment the level of inorganic as well as organic mercury accumulated in kidneys and liver was estimated. After a 12-week exposure, sodium selenite decreased the level of total mercury in the liver (in the case of both EtHg and PhHg: from 47.0 to 31.8 and from 41.3 to 25.4 micrograms Hg/g tissue, respectively). It also slightly decreased the mercury level in the kidneys of animals exposed to PhHg (from 889 to 73.3 micrograms Hg/g tissue) but did not change the mercury concentration in the kidneys of guinea pigs exposed to ethylmercuric chloride.
Animals↗
[Pharmacokinetic study of sodium selenite in low-selenium rabbits].
Sodium selenite has been used for prevention and treatment of Keshan disease and Kaschin-Beck's disease. The efficacious dosage regimens of sodium selenite in low-Se human body have not been clear. A single iv or ig of sodium selenite 2.0 mg/kg was given to rabbits. Selenium in whole blood was determined fluorophotomerically. The concentration-time curve following a single iv of sodium selenite in rabbits was found to be of 3-compartment open model. The pharmacokinetic parameters were: T1/2 x 0.11 +/- 0.03 h, T1/2 alpha 6.8 +/- 2.8 h, T1/2 beta 215 +/- 35 h, Vc 0.50 +/- 0.07 L/kg, Cl 19 +/- 5 ml/(kg.h), AUC 146 +/- 26 mg.h/L. The concentration-time curve following a single ig of sodium selenite showed a pattern of 2-compartment open model. The parameters were: T1/2 kappa a 13 +/- 6 h, T1/2 alpha 3.6 +/- 1.9 h, T1/2 beta 338 +/- 107 h, Vc 2.9 +/- 1.3 L/kg, AUC 78 +/- 29 mg.h/L, Cl 27 +/- 11 ml/(kg.h). In low-Se rabbits the distribution in body was more rapid and more extensive, and the bioavailability was higher than that in normal-Se rabbits. Therefore, attention should be paid to the different levels of selenium during therapy with sodium selenite.
Animals↗
[The in vitro inhibitory effect of sodium selenite on complement activation].
Sodium selenite exerts a marked inhibiting effect on the hemolysis induced by complement fixation. The results of rocket immunoelectrophoresis tests for the activated fragments C3d and C4d show that sodium selenite inhibits complement activation through the alternative pathway.
Complement Activation↗
Labeling of the neurons of origin of zinc-containing pathways by intraperitoneal injections of sodium selenite.
Intraperitoneal injections of sodium selenite result in the formation of zinc-selenium complexes in zinc-containing axonal boutons ("Timm stainable boutons"), and the zinc-selenium precipitate can be rendered visible in histological sections by silver enhancement. In this work we present evidence, in the rat, that zinc-selenium precipitates formed in vivo after intraperitoneal injections of sodium selenite are translocated by colchicine-sensitive retrograde transport to neural perikarya when animals are allowed to survive 12-24 h after the selenite administration. Silver enhancement renders the perikaryal precipitates visible and thus demonstrates the perikarya of all zinc-containing neurons in the CNS simultaneously. Large populations of zinc-containing neurons identified by the method are found in layers II, III, and VI of all neocortical areas, in the superficial and deep layers of the prepyriform areas and, with a high degree of regional differentiation, in the retrosplenial, entorhinal, para- and presubicular cortices, the hippocampal formation and the amygdaloid complex. Zinc-containing cells were absent from the caudate-putamen, nucleus accumbens and septal complex. Labeled zinc-containing cells are absent in non-telencephalic parts of the brain. The findings indicate that the zinc-containing circuitry of the brain mainly serves in telencephalic information processing.
Animals↗
Antioxidative and immunomodulatory role of melatonin, sodium selenite, N-acetyl-L-cysteine and quercetin on human umbilical blood.
We have previously reported on the DNA oxidative damage and oxygen stress in healthy term neonates. The aim of the present study was to investigate the antioxidative and immunomodulatory role of melatonin, sodium selenite, N-acetyl-L-cysteine and quercetin on umbilical blood. The single cell gel electrophoresis (comet) assay was used for DNA oxidative damage. The lymphocytes proliferation and natural killer (NK) activity in umbilical blood were assayed by 3[H]-thymidine uptaken and MTT methods. Results using comet assay showed protection by melatonin, N-acetyl-L-cysteine (NAC) and quercetin, and a protective and damaging effect by selenite sodium. Melatonin, sodium selenite, NAC and quercetin greatly promoted the lymphocytes proliferation to IL-2. NK activity of the umbilical blood was significantly increased by melatonin and sodium selenite, but was not affected by NAC and quercetin. These data suggest that antioxidants are able to protect umbilical blood mononuclear cells against oxygen stress and affect oxygen stress mediated immune function inhibition of umbilical blood. These results will supply new experimental data for using umbilical blood to treat diseases.
Acetylcysteine↗