Arsenic accumulation and metabolism

M. J. Abedin, M. S. Cresser, A. A. Meharg, J. Feldmann, J. Cotter-Howells, Arsenic accumulation and metabolism in rice (Oryza sativa L.). Environ. Set Technol., 36 (2002), 962D 968. 

TABLE 4. Arsenic accumulation and metabolism in three-step freshwater food chain ... 

TABLE 5. Arsenic accumulation and metabolism in three-step freshwater food chain (phytoplankton Nostoc sp - shrimp N. denticulata carp C. carpio) [51]... 

Hughes, M.F., Kenyon, E.M., Edwards, B.C. et al. (2003) Accumulation and metabolism of arsenic in mice after repeated oral administration of arsenate. Toxicology and Applied Pharmacology, 191(3), 202-10. 

In strains dependent on Pit for inorganic phosphate uptake, exposure to arsenate leads to the depletion of intracellular adenosine triphosphate (ATP) stores and the intracellular accumulation of arsenate, demonstrating the direct interference of arsenate in phosphate metabolism (4). 

As is the case with isotopic labeling of molecules, enriched levels of stable isotopes of elements can be used as tracers. Isotopes of elements can be used as nutritional supplements for plants or animals to trace absorption, assimilation, and metabolism of elements (Allen and Georgitis). Processes such as biomethylation of elements like mercury and arsenic in the environment can be studied using isotopically enriched elements. In some cases, methylated metals are more toxic than the inorganic species, and generally accumulate up the food chain. 

In order for this enzyme to work, a chemical known as S-adenosylmethionine (SAM) must be present in the liver. SAM is a derivative of the aunino acid methionine, which is essential to our health. There is only a certain amount of SAM in our liver that is available to combine with arsenic and render it nontoxic. If more au senic enters the liver than the amount of available SAM can handle, then excess non-metabolized au"-senic may accumulate in the liver and be distributed to other orgams, causing toxic effects. This is known ais metabolic saturation. As long as the aunount of arsenic (i.e., the dose) is below this saturation level, our liver can detoxify it and no toxic effects will result. It is only when the amount of arsenic overwhelms the metabolic pathway that toxic effects can develop. This illustration of a threshold below which toxic effects do not occur is a key concept in toxicology (see chapter 3 for a graphical illustration of the threshold concept). 

The principal controls on the microbial reaction rate in our example, then, are biomass and thermodynamic drive (Fig. 33.2). Initially, in the presence of abundant lactate and arsenate, the rate is controlled by the size of the microbial population available to catalyze lactate oxidation. As the population increases, so does reaction rate. Later, as reactants are consumed and products accumulate, the reaction approaches the point at which the energy liberated by its progress is balanced by that needed in the cell to synthesize ATR Reaction rate is governed now by the energy available to drive forward the cellular metabolism, this energy represented by the thermodynamic potential factor Ft over the course of the experiment, the kinetic factors Fd and Fa play minor roles. 

In metabolic studies with animals it is often difficult to distinguish between processes carried out by the animal and those performed by resident microorganisms, such as the gut microflora. In the following, the transformations refer to those taking place within the marine animal, whether microbially mediated or otherwise. Metabolic studies with marine animals are faced with further complications because water can be an important uptake route. A chemical, in this instance arsenic in its various forms, may undergo microbial conversions in the water, and the resultant metabolites may be accumulated by the marine animal. Thus, careful experimentation may be required to determine what is occurring inside rather than outside the animal. 

Overall Metabolic Processes. In general, metabolic processes which facilitate elimination of a pesticide from the body are considered desirable. This is based a great deal on our long history of associating toxicity with chemicals that accumulate in the body. Arsenic, lead, mercury and other metals substantiate these concerns as do more modern synthetic organic chemicals such as DDT and mirex. Because so many chemicals rapidly voided from the body are now known to be extremely hazardous, risks and excretion rates are evaluated very carefully. Still, storage of metabolites is not a positive characteristic even for those compounds like DDE whose danger, if any, as a body burden has not been established. 

Arsenic occurs naturally in small amounts in many foods. Shrimp, for example, contain about 19 parts per million (ppm) arsenic, and corn may contain 0.4 ppm arsenic. The amount of naturally occurring arsenic in foods depends on the surroundings where they are grown and the metabolism of the plant or animal. While many soils contain arsenic, which causes an accumulation of the element as a plant grows, some insecticides also contain arsenic, which causes an arsenic residue when the insecticide is applied. The U.S. Food and Drug Administration (FDA) has set a limit of 76 ppm for arsenic levels in shellfish. In its ionic forms, arsenic is much more toxic than in its covalently bound compounds. The typical toxic arsenic compounds contain ions such as arsenate (AsO ) or arsenite (AsOg). 

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