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IGF and GH mRNA levels are suppressed upon exposure to micromolar concentrations of cobalt and zinc in rainbow trout white muscle

Date

2011

Author

Ekinci, Deniz
Ceyhun, Saltuk Bugrahan
Aksakal, Ercument
Erdogan, Orhan

Metadata

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Abstract

The objective of this study was to assess the effects of cobalt and zinc exposure of rainbow trout (Oncorhynchus mykiss) on insulin like growth factors (IGF) and growth hormone (GH). Mature rainbow trouts were exposed to 0.42, 2.1, 4.2. 21 and 42 mu mol/L Co2+ (added as CoCl2 center dot 6H(2)O) and 0.34, 1.7, 3.4, 17 and 34 mu mol/L Zn2+ (added as ZnSO(4)i center dot 7H(2)O). After 6, 12,24 and 48 h of treatment, expressions of white muscle IGF-I, IGF-II and GH mRNAs were measured by means of quantitative Real Time PCR. During the exposure experiments, no mortalities occurred. The most effective metal concentrations, which caused significant alterations, were determined to be 42 mu mol/L Co2+ (10 mg CoCl2 center dot 6H(2)O/L) and 3.4 mu mol/L Zn+2 (1 mg ZnSO4 center dot 7H(2)O/L). The following results were obtained for these concentrations. Expression of IGF-I did not change at 6 h in zinc treatment while the decrease (p < 0.05) was observed at 12 h and 24 h, and this decrease became stronger at 48 h. Cobalt exposure caused a decrease in IGF-I mRNA level at 6 h, 12 h, 24 h and 48 h (p < 0.05). Both zinc and cobalt exposure resulted in significant decreases in GH expression at 6 h. Exposure of trout to Zn resulted in a decrease in expression of IGF-II starting from 6 h whereas the significant decrease started at 6 h in cobalt exposure and this decrease elevated at 24 h. The results indicate that micromolar cobalt and zinc exposure causes significant attenuation in the expressions of these three genes' time dependently. Our findings show that IGF-I is the most resistant and GH is the most sensitive component against cobalt and zinc exposure. We conclude that IGF/GH axis might be strongly affected by the short term exposure to low micromolar concentrations of zinc and cobalt due to alterations of these genes. (C) 2010 Elsevier Inc. All rights reserved.

Source

Comparative Biochemistry and Physiology C-Toxicology & Pharmacology

Volume

153

Issue

3

URI

https://doi.org/10.1016/j.cbpc.2010.12.004
https://hdl.handle.net/20.500.12712/17276

Collections

  • PubMed İndeksli Yayınlar Koleksiyonu [6144]
  • Scopus İndeksli Yayınlar Koleksiyonu [14046]
  • WoS İndeksli Yayınlar Koleksiyonu [12971]



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