Pathological Effects
41
erly, either as components of cellular structure (tissue synthesis) or as
enzymes in cellular metabolism. Selenium is similar to sulfur in its
basic chemical and physical properties (has same valence states and
forms analogs of hydrogen sulfide, thiosulfate, sulfite, and sulfate),
and mammalian studies show that cells do not discriminate well between the two as proteins are being synthesized (it is assumed that the
mechanistic features underlying toxicity are essentially the same for
fish, since the resulting pathology and teratogenic features are the
same). When present in excessive amounts, selenium is erroneously
substituted for sulfur, resulting in the formation of a triselenium linkage (Se-Se-Se) or a selenotrisulfide linkage (S-Se-S), either of which
prevent the formation of the necessary disulfide chemical bonds (S-S).
Distorted, dysfunctional enzymes and protein molecules, which impair normal cellular biochemistry, are the end result (Ganther 1974;
Stadtman 1974; Diplock and Hoekstra 1976; Reddy and Massaro 1983;
Sunde 1984). Thus, while selenium is a sulfur analog in some respects, its biochemistry and potential toxicity are quite different.
Selenium-induced errors in protein biosynthesis can have several
outcomes. The most well documented overt toxic symptom in fish is
reproductive teratogenesis. Selenium consumed in the diet of adult
fish is deposited in the eggs, where it is metabolized by larval fish after
hatching. A variety of lethal or sublethal deformities can occur in the
developing fish, affecting both hard and soft tissues (Lemly 1993a).
Substitution of selenium for sulfur can also impair proper formation of
proteins in juvenile and adult fish, and many internal organs and tissues can develop pathological alterations that are symptomatic of
chronic selenosis (Sorensen 1986). Studies in mammals and waterfowl
show that acute toxic responses may also involve tissue damage from
bioreactive superoxides produced in response to high concentrations of
selenium (O'Toole and Raisbeck 1998). At the subcellular level, selenium poisoning disrupts enzyme-mediated biochemical reactions thus
impairing metabolism. This impairment can result in the death of cells
and the entire organism (Stadtman 1974, Diplock and Hoeckstra 1976).
Pathological Effects
Gills
The primary structure of adult teleost gills is the semicircular gill arch;
there are usually 4 gill arches on each side of the head. Each arch
contains a double row of filaments, and each filament has a row of
microscopic lamellae projecting from each side (Fig. 3.2). The lamellae contain the blood sinusoids and capillary beds and are covered by a
thin epithelial cell layer, typically 2-cells thick, underlain by support-
41
erly, either as components of cellular structure (tissue synthesis) or as
enzymes in cellular metabolism. Selenium is similar to sulfur in its
basic chemical and physical properties (has same valence states and
forms analogs of hydrogen sulfide, thiosulfate, sulfite, and sulfate),
and mammalian studies show that cells do not discriminate well between the two as proteins are being synthesized (it is assumed that the
mechanistic features underlying toxicity are essentially the same for
fish, since the resulting pathology and teratogenic features are the
same). When present in excessive amounts, selenium is erroneously
substituted for sulfur, resulting in the formation of a triselenium linkage (Se-Se-Se) or a selenotrisulfide linkage (S-Se-S), either of which
prevent the formation of the necessary disulfide chemical bonds (S-S).
Distorted, dysfunctional enzymes and protein molecules, which impair normal cellular biochemistry, are the end result (Ganther 1974;
Stadtman 1974; Diplock and Hoekstra 1976; Reddy and Massaro 1983;
Sunde 1984). Thus, while selenium is a sulfur analog in some respects, its biochemistry and potential toxicity are quite different.
Selenium-induced errors in protein biosynthesis can have several
outcomes. The most well documented overt toxic symptom in fish is
reproductive teratogenesis. Selenium consumed in the diet of adult
fish is deposited in the eggs, where it is metabolized by larval fish after
hatching. A variety of lethal or sublethal deformities can occur in the
developing fish, affecting both hard and soft tissues (Lemly 1993a).
Substitution of selenium for sulfur can also impair proper formation of
proteins in juvenile and adult fish, and many internal organs and tissues can develop pathological alterations that are symptomatic of
chronic selenosis (Sorensen 1986). Studies in mammals and waterfowl
show that acute toxic responses may also involve tissue damage from
bioreactive superoxides produced in response to high concentrations of
selenium (O'Toole and Raisbeck 1998). At the subcellular level, selenium poisoning disrupts enzyme-mediated biochemical reactions thus
impairing metabolism. This impairment can result in the death of cells
and the entire organism (Stadtman 1974, Diplock and Hoeckstra 1976).
Pathological Effects
Gills
The primary structure of adult teleost gills is the semicircular gill arch;
there are usually 4 gill arches on each side of the head. Each arch
contains a double row of filaments, and each filament has a row of
microscopic lamellae projecting from each side (Fig. 3.2). The lamellae contain the blood sinusoids and capillary beds and are covered by a
thin epithelial cell layer, typically 2-cells thick, underlain by support-