Detoxification selenium

Kessi J, Ramuz M, Wehrh E, et al. 1999. Reduction of selenite and detoxification of elemental selenium by the phototrophic bacterium Rhodospirillum rubrum. Appl Environ Microbiol 65 4734-40. 

Heavy metals stimulate or inhibit a wide variety of enzyme systems (16, 71, 72), sometimes for protracted periods (71, 73). These effects may be so sensitive as to precede overt toxicity as in the case of lead-induced inhibition of 8 ALA dehydrase activity with consequential interference of heme and porphyrin synthesis (15, 16). Urinary excretion of 8 ALA is also a sensitive indicator of lead absorption (74). Another erythrocytic enzyme, glucose-6-phosphatase, when present in abnormally low amounts, may increase susceptibility to lead intoxication (75), and for this reason, screens to detect such affected persons in lead-related injuries have been suggested (76). Biochemical bases for trace element toxicity have been described for the heavy metals (16), selenium (77), fluoride (78), and cobalt (79). Heavy metal metabolic injury, in addition to producing primary toxicity, can adversely alter drug detoxification mechanisms (80, 81), with possible secondary consequences for that portion of the population on medication. 

Crocker sarcoma and Mecca lymphosarcoma tumors were found to accumulate the radioselenium slowly and continuously in contrast to rapid uptake and clearance of the label from most normal organs. Clinically, the affinity of tumors for selenium has been the basis for utilizing a radioactive nuclide of selenium as a tumor localizing agent (62, 64) The reason for the localization of selenium is not readily apparent but may reflect enhanced division rates, protein and chondroitin sulfate biosynthesis, or a decrease in the detoxification of selenium. An outgrowth of these observations has been to examine the in vitro effects of selenium supplementation on cellular propagation. 

R. Martoja, D. Viale, Accumulation of mercuric selenide granules in the liver of Odontocetes (mammifer cetaced) a possible method of detoxification of methymer-cury by selenium, Comp. Rend. Hebdom. Sean., Paris, Series D Sci. Natur., 285 (1977), 109-112. 

In a case-control study in 106 heroin-dependent individuals undergoing an opioid detoxification program (n = 19) or a methadone maintenance treatment program (n = 87) there were large significant differences in the mean values of some vitamins and minerals between the heroin-dependent individuals and the healthy, non-dependent controls (37). Dependent individuals had higher white cell counts and transaminases and lower erythrocyte counts and cholesterol, albumin, tocopherol, folic acid, sodium, selenium, and copper concentrations. 

The metabolic product of the metal can determine the action in the organ in which the metal is deposited. Usually, metabolism of metals can lead to detoxification and often to excretion. Some metals, such as selenium metal and oxides, are converted to the volatile trimethyl derivative and are exhaled. On the other hand, mercury is converted to methyl mercury chloride, which is soluble in lipids and appears to be concentrated overtime in organs with high lipid content. 

Dimethyl selenide is exhaled, and the trimethylselenonium ion is a major urinary metabolite of selenium. Methylation of selenium is a detoxification pathway that is especially important at high selenium doses. 

Excretion of selenium by humans occurs in the urine, feces, expired air, and sweat, but urine and feces are the major routes of elimination. Some of the selenium in feces may be due to bilary excretion (Levander and Baumann 1966a, 1966b). Elimination is reduced in selenium-deficient individuals and may represent a mechanism by which selenium levels are regulated (Martin et al. 1989a Swanson et al. 1991). Methylation is an important mechanism of detoxification for selenium dimethyl selenide is exhaled, and the trimethylselenonium ion is the major urinary metabolite of selenium. Experiments in mice suggest that the hepatic toxicity of selenium may be at least partly due to depression of selenium methylation in the liver, resulting in the accumulation of excess selenides (Nakamuro et al. 2000). 

A susceptible population will exhibit a different or enhanced response to selenium than will most persons exposed to the same level of selenium in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). These parameters result in reduced detoxification or excretion of selenium, or compromised function of organs affected by selenium. Populations who are at greater risk due to their unusually high exposure to selenium are discussed in Section 6.7, Populations With Potentially High Exposures. 

Horne AJ. 1991. Selenium detoxification in wetlands by permanent flooding I. Effects on a macroalga, an epiphytic herbivore, and an invertebrate predator in the long-term mesocosm experimental at Kesterson Reservoir, California. Water Air Soil Pollut 57-58 43-52. 

Zhang X, Yang G, Gu L. 1991. Detoxification mechanism of methionine and vitamin E in selenium toxicity in rats. Acta Nutrimenta Sinica 13(l) 32-38. 

Yoneda S and Suzuki KT (1997) Detoxification of mercury by selenium by binding of equimolar Hg-Se complex to a specific plasma protein. Toxicol Appl Pharmacol 143 274-280. 

The presence of these novel selenosugars has also raised the issue of their possible toxicity. It is generally thought that TMSe is the product of a detoxification process designed to remove excess, potentially toxic inorganic selenium. Toxicity studies showing that TMSe is considerably less toxic than selenite have supported this view. This appears to also apply to the selenosugars which were shown in cytotoxicity studies to be 1,000-fold less toxic than selenite. ... 

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