Skip to main content

Published 2007

Read in Norwegian

Publication details

Journal : Aquaculture International , vol. 15 , p. 43–54 , 2007

Publisher : Springer

International Standard Numbers :
Printed : 0967-6120
Electronic : 1573-143X

Publication type : Academic article

Contributors : Cooper, Marie; Midling, Kjell Øyvind

If you have questions about the publication, you may contact Nofima’s Chief Librarian.

Kjetil Aune
Chief Librarian
kjetil.aune@nofima.no

Summary

Melanin deposits in white muscle represent a potentially serious quality problem for farmed cod. Black lines of deposited melanin are associated with blood vessels and consist of layers of melanin-filled cells. Despite numerous anecdotal reports of melanosis in farmed cod no detailed investigations into the underlying mechanisms have been undertaken. In this study we have confirmed that melanosis is present in both farmed and wild cod. However, the incidence of melanosis in wild fish is much lower than that in farmed fish. In addition, we have demonstrated that tyrosinase, a copper-dependent metalloenzyme that is the primary enzyme of melanin synthesis, is present in cod tissues. Copper levels are significantly different in the white muscle of farmed (0.5 ± 0.03 mg/kg wet weight) and wild (0.34 ± 0.01 mg/kg wet weight) cod (P < 0.05) and in the blood vessels of farmed (2.23 ± 0.37 mg/kg wet weight) and wild (0.32 ± 0.02 mg/kg wet weight) cod (P < 0.05). Similarly, differences in the levels of tyrosinase activity were observed in both muscle and blood vessels. Melanised tissues contain higher copper concentrations than tissue containing little or no melanin. Furthermore,
we have shown that the addition of copper to protein extracts from fish muscle causes an increase in tyrosinase activity in vitro. Our results suggest that overabundance of copper in commercial feeds leads to increased melanin synthesis via
increased tyrosinase activity. We propose that melanin is deposited at sites of high copper exposure and subsequently sequesters copper as a means of reducing the overload stress on other homeostatic mechanisms.