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

Citation
Mhg. Berntssen et al., Tissue metallothionein, apoptosis and cell proliferation responses in Atlantic salmon (Salmo salar L.) parr fed elevated dietary cadmium, COMP BIOC C, 128(3), 2001, pp. 299-310
Citations number
56
Categorie Soggetti
Pharmacology & Toxicology
Journal title
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
ISSN journal
15320456 → ACNP
Volume
128
Issue
3
Year of publication
2001
Pages
299 - 310
Database
ISI
SICI code
1532-0456(200103)128:3<299:TMAACP>2.0.ZU;2-L
Abstract
Atlantic salmon parr were reared for 4 months on experimental diets supplem ented with 0 (control), 0.5, 5, 25, 125, or 250 mg Cd kg(-1) feed to establ ish a threshold concentration for dietary cadmium exposure by assessing ear ly adaptive cellular responses. At the end of the experiment, the lowest di etary Cd concentration that caused significant accumulation in the gut, kid ney and muscle was 5 mg Cd kg(-1) compared to the control group. Over time, dietary Cd accumulated first in the gut (after 1 month), followed by the k idney (2 months), and later by muscle (4 months). Highest Cd accumulation ( 100-fold) was found in the gut. A significant increase in regulated cell de ath and proliferation in salmon fed 125 mg Cd kg(-1) compared to control fi sh appeared efficient in preventing gross histopathological damage in the i ntestine. The highest increase in metallothionein levels was found in the k idney, and metallothionein (MT) levels increased disproportionally to Cd ac cumulation at increased exposure concentrations. It was concluded that MT w as 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 incre ase in metallothionein, EC50) of 7 mg Cd kg(-1), indicating toxic exposure at this concentration. (C) 2001 Elsevier Science Inc. All rights reserved.