Acclimation to Copper by Rainbow Trout,Salmo gairdneri: Biochemistry

Abstract

Whole body, gill, and liver copper uptake, gill Na+-K+-ATPase specific activity, and gill and liver acid-soluble thiols (AST), glutathione, and cysteine of rainbow trout (Salmo gairdneri) were measured during 28 d of exposure to 55 μg copper∙L−1. Na+-K+-ATPase specific activity was inhibited by 33% within 24 h of copper exposure, but this was compensated by a significant increase in microsomal protein so that the total Na+-K+-ATPase activity per milligram of gill tissue returned to normal by day 14. There was no accumulation of copper and no increase in AST, glutathione, or cysteine in the gill. However, after 7 d of exposure, hepatic AST and glutathione had increased by about 2 times, and a sulfhydryl-rich, acid-soluble protein, tentatively identified as metallothionein, increased by 2.8 times. Copper accumulation was highest in the liver, but other tissues also accumulated copper.

Interactions between copper and cadmium modify metal organ distribution in mature tilapia, Oreochromis mossambicus

“…The metal accumulation in the intestinal wall might be a specific mechanism for tilapia, because in general in fish about 95% of the whole body Cu accumulation was allocated into the liver (Stagg and Shuttleworth, 1982;Laurrn and McDonald, 1987). Perhaps an efficient accumulation and excretion route via the intestine contributes to the metal tolerance of tilapia, which is higher than in other species studied.…”

“…This accumulation was concentration-and time-dependent, only for Cd. Increased metal concentrations were also observed in Cu-exposed carp, brown bullhead and roach (Yamamoto et al, 1977;Stagg and Shuttleworth, 1982;Segner, 1987) but not in rainbow trout (Laurrn and McDonald, 1987), and in Cd-exposed rainbow trout, pike and American eel (Brown et al, 1986;Norey et al, 1990;Gill et al, 1992). Metal-metal interactions after single metal exposure were shown by Gill et al (1992) who reported an increased Cu concentration in the gills of eels after Cd exposure.…”

Integrated physiological response of tilapia, Oreochromis mossambicus, to sublethal copper exposure

“…In flounder, Stagg and Shuttleworth (1982b) observed no effect after in vivo Cu exposure, whereas Lauren and McDonald (1987) observed in trout an inhibition of N a 7 K + -ATPase specific activity, which was compensated by an S. M. G.J. Pelgrom et al I Aquatic Toxicology 32 (1995) 303-320 317 increase in the microsomal protein concentration.…”

Copper acclimation in juvenile fathead minnows: Is a cycle of branchial damage and repair necessary?

“…The branchial damage can include: a reduction in Na + influx McDonald, 1985, 1987a) a stimulation of Na + efflux (Laurén and McDonald, 1985) and an inhibition of branchial Na + -K + ATPase activity (Stagg and Shuttleworth, 1982;Laurén and McDonald, 1987b;Pelgrom et al, 1995;Kolok et al, 2002). These branchial changes can lead to an increase in net Na + loss (Croke and McDonald, 2002;Taylor et al, 2004), which can culminate in a significantly reduced concentration of whole-body Na + (Laurén and McDonald, 1987a;McGeer et al, 2000;Kolok et al, 2002).…”

“…These branchial changes can lead to an increase in net Na + loss (Croke and McDonald, 2002;Taylor et al, 2004), which can culminate in a significantly reduced concentration of whole-body Na + (Laurén and McDonald, 1987a;McGeer et al, 2000;Kolok et al, 2002). The damage phase is often followed by a repair phase during which Na + influx rates are restored (Laurén and McDonald, 1987a), efflux rates are reduced (Laurén and McDonald, 1987a), and Na + -K + ATPase specific activity are adjusted levels that are consistent with (Laurén and McDonald, 1987b) or in excess of pre-exposure levels. As a consequence of these acclimatory changes, there can be a recovery of whole-body Na + to pre-exposure levels (Laurén and McDonald, 1987a;McGeer et al, 2000).…”