Tissue metallothionein, apoptosis and cell proliferation responses in Atlantic salmon (Salmo salar L.) parr fed elevated dietary cadmium.

Atlantic salmon parr were reared for 4 months on experimental diets supplemented with 0 (control), 0.5, 5, 25, 125, or 250 mg Cd x kg(-1) feed to establish a threshold concentration for dietary cadmium exposure by assessing early adaptive cellular responses. At the end of the experiment, the lowest dietary Cd concentration that caused significant accumulation in the gut, kidney and muscle was 5 mg Cd x kg(-1) compared to the control group. Over time, dietary Cd accumulated first in the gut (after 1 month), followed by the kidney (2 months), and later by muscle (4 months). Highest Cd accumulation (100-fold) was found in the gut. A significant increase in regulated cell death and proliferation in salmon fed 125 mg Cd x kg(-1) compared to control fish appeared efficient in preventing gross histopathological damage in the intestine. The highest increase in metallothionein levels was found in the kidney, and metallothionein (MT) levels increased disproportionally to Cd accumulation at increased exposure concentrations. It was concluded that MT was not directly associated with long-term Cd accumulation. Atlantic salmon showed increased metallothionein levels in the kidney at a median effective concentration (concentration of dietary Cd giving 50% of the maximum increase in metallothionein, EC50) of 7 mg Cd x kg(-1), indicating toxic exposure at this concentration.