An inverse relationship between serum Se levels and cancer risks has been reported. Create . Formula: It is an oxoacid of selenium, and its structure is more accurately described as (HO) 2SeO 2. Under sulfidogenic conditions, chemical precipitation is operated in preference to enzymatic reduction, and D. desulfuricans was able to precipitate Tc extracellularly, probably as sulfide. The capacity of SRB to reduce and solubilize As and for soluble As(III) to precipitate with sulfide has further potential for bioremediation. It is an oxoacid of selenium, and its structure is more accurately described as 2SeO 2. It follows, given such a mechanism, that expression of selenium-dependent genotoxic activity is likely to be concentration and threshold dependent, but this remains to be shown. 1 Structures Expand this section. Molecular Geometry. Sodium selenate CAS Number: 13410-01-0 Molecular formula: Na2SeO4 IUPAC Name: disodium selenate. 2. In the body, selenium is an important component of several selenoproteins such as the antioxidant family of glutathione peroxidases as well as other enzymes such as the iodothyronine deidodinases and thioredin reductases. List of Selenate Compounds, Common Compounds of Selenate SeO4, Formula, Molecular Weight Reduction of TeO32− to Te0 is also a means of detoxification found in bacteria and fungi, with Te0 being deposited in or around the cells, resulting in black colonies. The molecular structure and the atom-numbering scheme of the title compound are shown in Fig. 2021-02-07. It was also suggested that inhibition of DNA methyltransferase may be a major mechanism of chemoprevention by selenium compounds at the post-initiation stage of carcinogenesis [43]. Potassium Selenate K2SeO4 Molar Mass, Molecular Weight. The reduction of selenate (Se(VI)) and selenite (Se(IV)) to elemental selenium can be catalyzed by numerous microbes, which can result in a red precipitate deposited around the cells and colonies. Doses of 0.3, 0.6, 1, and 2 mg Se/kg bw did not cause any clastogenic effects. Finally, SerC is thought to encode a b-type cytochrome located in the periplasm in analogy to DdhC from Rhodovulum sulfidophilum. Download : Download high-res image (130KB) Download : Download full-size image; Fig. Cherest et al., 1997; El Kassis et al., 2007; Shibagaki et al., 2002; Smith et al., 1995a, Fitzpatrick et al., 2008; Tomatsu et al., 2007, Handbook on the Toxicology of Metals (Third Edition). The inorganic [HSeO 4] − and H 2 SeO 4 species consist of infinite two-dimensional inter-linkers via strong hydrogen bonds (O-H⋯O), giving birth to trimmers [ (H 2 SeO 4) 2 HSeO 4] nn−. Itoh and Shimada (1996) reported similar findings. No specific recommendations have been reported for reducing absorption after acute high-dose exposure to selenium or selenium compounds via inhalation or dermal exposure. JOHAN HÖGBERG, JAN ALEXANDER, in Handbook on the Toxicology of Metals (Third Edition), 2007. Therefore, selenium concentrations in foods are dependent on the selenium content of the soil in which the foods or ingredients were grown. Clinical efficacy of selenium, including its chemopreventive effects, derives from the activities of intracellular selenium metabolites, including methyl selenol (reviewed in Ref. It was a double-blind randomized study focusing on the prevention of recurrent skin tumors in participants dosed with 200 μg selenium/day in the form of selenium-enriched yeasts. It is a conjugate base of an arsenate(2-). Justify your choice(s) by showing the Lewis structure and stating the geometry for EACH pair (you must also show why certain pairs were NOT chosen). Compare bond angle predictions from the VSEPR-based model to real molecules. PurposeQuest International . The study did not demonstrate any positive effect of selenium supplementation on recurrent skin tumors, but yielded data on a significant reduction in the occurrence of prostate, lung, and colon cancers (Duffield-Lillico et al., 2002). Additionally, selenium deficiency was found to decrease both global DNA methylation and methylation in the promoter region of the p53 gene in Caco-2 cells and rat liver and colon cells [44].