Bioaccumulation and Hepatic Speciation of Copper in Rainbow Trout (Oncorhynchus mykiss) During Chronic Waterborne Copper Exposure

Abstract

To protect cells from toxicity, metal-sensitive cellular compartments must be insulated against essential but toxic metals [such as copper (Cu)] accumulated in excess of metabolic requirements. We measured Cu concentrations at the organ and hepatic subcellular levels in juvenile rainbow trout (Oncorhynchus mykiss) during exposure to sublethal waterborne Cu (40 microg/L) for 21 days. There was a time-dependent accumulation of Cu in the gill, liver, plasma, and carcass, with significant difference in Cu-exposed fish relative to the controls being evident by day 7. This significant accumulation of Cu was not associated with impaired growth. Copper concentrations in purity-tested liver subcellular fractions normalized to the liver protein concentration were in decreasing order: organelles > heat-stable proteins > nuclei-debris > NaOH-resistant granules > heat-labile proteins. As a proportion of the total, the majority of the hepatocellular Cu burden (60-68%) was associated with a metabolically active pool (organelles, nuclei-debris, and heat-stable proteins) and the remainder (32-40%) was associated with a metabolically detoxified pool (heat-stable proteins and NaOH-resistant granules) irrespective of the Cu-exposure regime. Because Cu concurrently accumulated in metabolically active and detoxified pools, we conclude that the spillover hypothesis of metal toxicity did not hold under the exposure conditions employed in this study. Moreover, these data suggest that rainbow trout can withstand significant above-background Cu accumulation in hepatic putative metal-sensitive compartments without chronic toxic effects at the organism level.

Biochemical, haematological and oxidative stress responses of common carp (Cyprinus carpio L.) after sub-chronic exposure to copper

“…The liver is the main organ responsible for the maintenance of copper homeostasis and is also a possible target for copper-induced damage in fish (Grosell et al 1998;Abdel-Tawwab et al 2007;Kamunde and McPhail 2008). In our study, we observed hydropic and vacuolar degeneration of hepatocytes, the dilatation of capillaries, mild hyperaemia, and cholestasis.…”

Gene expression and TNF-alpha secretion profile in rainbow trout macrophages following exposures to copper and bacterial lipopolysaccharide

“…The copper concentrations selected for the main experiment (1, 10 and 50 mM) took into account the cell viability results and the knowledge that fish captured at impacted sites had concentrations in plasma that reach 50 mM [22].…”

Protein carbonyls and antioxidant defenses in corkwing wrasse (Symphodus melops) from a heavy metal polluted and a PAH polluted site

“…Other binding sites may be involved in metal chelation in corkwing wrasse, thereby eliminating the need for MT induction. Kamunde and MacPhail (2008) found indiscriminate Cu binding in all subcellular fractions of rainbow trout liver suggesting that Cu-binding sites are ubiquitous in this organ. Also, base-line levels of MT in corkwing wrasse may be sufficient to counteract the metal exposure at this site.…”