Pathology of selenium poisoning in fishAuthor(s): A. Dennis Lemly
Source: In: Frankenberger, Jr., William T.; Engberg, Richard A., eds. Environmental chemistry of selenium. New York: Marcel Dekker, Inc.: 281-296.
Publication Series: Miscellaneous Publication
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DescriptionSelenium presents an interesting paradox in the field of aquatic toxicology because it is both a nutrient and a poison. As a nutrient, it is required in the diet of fish at concentrations of about 0. 1 to 0. 5 Fg/g dry weight. Selenium is necessary for proper formation and functioning of glutathione peroxidase, which is a major cellular antioxidant enzyme. This enzyme protects cell membranes from damage or lysis due to lipid peroxidation. Without adequate selenium, normal cellular and organ metabolism break down because of peroxides produced as a by-product of digestion. Symptoms of selenium deficiency in fish include reduced growth, anemia, exudative diathesis, muscular dystrophy, and increased mortality. Thus, the beneficial effects of proper selenium in the diet of fish are firmly established.
At dietary concentrations of only 7 to 30 times those required >3 Fg/g), selenium becomes a poison. Some of the major toxic effects are due to a simple principle of cell biology. From a biochemical perspective, selenium is very similar to sulfur, and cells do not discriminate well between the two when carrying out one of their key functionsCprotein synthesis. When present in excessive amounts, selenium is erroneously substituted for sulfur in proteins that are being formed inside the cells. Sulfur-to-sulfur linkages (ionic disulfide bonds) are necessary for protein molecules to coil into their tertiary (helix) structure which, in turn, is necessary for proper functioning of the protein, either as a cellular building block or as a component of enzymes. Substitution of selenium for sulfur disrupts the normal chemical bonding, resulting in improperly formed and dysfunctional proteins or enzymes.
Thresholds for dietary selenium toxicity in fish are easily reached and exceeded in contaminated aquatic systems. Excessive selenium can cause a wide variety of toxic effects at the biochemical, cellular, organ, and system levels. This chapter examines the most prominent outward manifestation of selenium toxicosisCteratogenic deformitiesCand discusses the use of this pathological symptom as a diagnostic tool for evaluating reproductive impairment and assessing impacts to fish populations in contaminated aquatic habitats.
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CitationLemly, A. Dennis. 1998. Pathology of selenium poisoning in fish. In: Frankenberger, Jr., William T.; Engberg, Richard A., eds. Environmental chemistry of selenium. New York: Marcel Dekker, Inc.: 281-296.
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