Page 324 - The Toxicology of Fishes

304 The Toxicology of Fishes

TABLE 6.4
a
Representative List of Stressors (Chemical and Nonchemical) Shown to Cause Oxidative Stress, Induce
b
Production of Reactive Oxygen Species, or Induce or Repress Antioxidant Defenses
Stressor (Common Examples) Refs.
Hydrogen peroxide Winzer et al. (2000, 2001)
Quinones (menadione, naphthoquinone, benzoquinone) Akerman et al. (2003); Petrivalsky et al. (1997);
Schmieder et al. (2003); Stephensen et al. (2002)
Aromatic nitro compounds (nitrofurantoin) Winzer et al. (2001)
Metals (cadmium, copper) Ariyoshi et al. (1990); Carvan et al. (2001);
Pedrajas et al. (1995); Radi and Matkovics
(1988); Rau et al. (2004)
PAHs (β-naphthoflavone, benzo(a)pyrene, 3-methylcholanthrene) Carvan et al. (2001); Hughes and Gallagher
(2004); Stephensen et al. (2002); Winzer et al.
(2000, 2001)
Pesticides (paraquat, endosulfan, dieldrin, malathion, chlorothalonil) Åkerman et al. (2003); Dorval et al. (2003);
Dorval and Hontela (2003); Elia et al. (2002);
Gallagher et al. (1992); Luo et al. (2005);
Pandey et al. (2001); Pedrajas et al. (1995)
Halogenated aromatic hydrocarbons (PCBs, dioxins) Carvan et al. (2001); Förlin et al. (1996);
Schlezinger and Stegeman (2001);
Schlezinger et al. (1999)
Ozone Ritola et al. (2002)
Hypoxia Cooper et al. (2002)
Hyperoxia Ritola et al. (2002)
Anoxia-reoxygenation Lushchak et al. (2001); Ross et al. (2001)
Heat stress Parihar and Dubey (1995); Parihar et al. (1996)
a As indicated by markers such as lipid peroxidation.
b As indicated in vitro either by dyes whose fluorescent properties are altered by exposure to ROS or by reporter
transgenes.
Note: Not all chemicals pertaining to the chemical classes listed are prooxidant; specific examples studied in the references
cited are listed in parentheses.

NADH than with NADPH as a source of reducing power, in contrast to the situation seen in rats (Jewell
and Winston, 1989; Kennish et al., 1989). Glutathione depletion under conditions of starvation was much
slower in mullet (Mugil cephalus) (Thomas and Wofford, 1984) and channel catfish (Ictalurus punctatus)
(Gallagher et al., 1992b) than in rodents. Perhaps because of the observed low (relative to rodents) rate
of turnover of glutathione in catfish, administration of buthionine sulfoximine (BSO), an inhibitor of
GCL, did not completely deplete hepatic glutathione, although coadministration of BSO and diethyl
maleate (DEM), a glutathione depletor, led to nearly complete depletion of glutathione (Gallagher et al.,
1992b). There is considerable variability in the reported catalytic activities of many of the antioxidant
enzymes, both between fish and mammals and between different fish species (Di Giulio et al., 1989;
Forlin et al., 1995; Gadagbui et al., 1996; Hasspieler et al., 1994a,b; Ploch et al., 1999; Rana and Singh,
1996; Winston, 1991). Biochemical differences that are important in terms of sample preparation and
treatment also exist; for example, mammalian CuZnSOD is a remarkably thermostable enzyme, but the
CuZnSODs from two different fish species are much more labile at high temperatures (60°C and above)
(Capo et al., 1997; Nakano et al., 1995). Vitamin E levels appear to be generally higher in fish cell
membranes than in mammalian cell membranes, but it is unclear whether this difference is protective
in the context of the typically higher levels of PUFA observed in fish cell membranes (Bell et al., 2000;
Singh et al., 1992). Some studies have found that fish cells are more resistant than mammalian cells to
oxidative stress in vitro (Singh et al., 1992; Venditti et al., 1999), while others have found the opposite
(Rau et al., 2004).