Iodine nutrition and toxicity in Atlantic cod (Gadus morhua) larvae

S Penglase,S Helland,K Hamre,T Harboe,Ø Sæle,A Nordgreen

doi:10.7717/peerj.20

S Penglase, S Helland + Show 4 more

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https://doi.org/10.7717/peerj.20

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Abstract

Copepods as feed promote better growth and development in marine fish larvae than rotifers. However, unlike rotifers, copepods contain several minerals such as iodine (I), at potentially toxic levels. Iodine is an essential trace element and both under and over supply of I can inhibit the production of the I containing thyroid hormones. It is unknown whether marine fish larvae require copepod levels of I or if mechanisms are present that prevent I toxicity. In this study, larval Atlantic cod (Gadus morhua) were fed rotifers enriched to intermediate (26 mg I kg-1 dry weight; MI group) or copepod (129 mg I kg-1 DW; HI group) I levels and compared to cod larvae fed control rotifers (0.6 mg I kg-1 DW). Larval I concentrations were increased by 3 (MI) and 7 (HI) fold compared to controls during the rotifer feeding period. No differences in growth were observed, but the HI diet increased thyroid follicle colloid to epithelium ratios, and affected the essential element concentrations of larvae compared to the other groups. The thyroid follicle morphology in the HI larvae is typical of colloid goitre, a condition resulting from excessive I intake, even though whole body I levels were below those found previously in copepod fed cod larvae. This is the first observation of dietary induced I toxicity in fish, and suggests I toxicity may be determined to a greater extent by bioavailability and nutrient interactions than by total body I concentrations in fish larvae. Rotifers with 0.6 mg I kg-1 DW appeared sufficient to prevent gross signs of I deficiency in cod larvae reared with continuous water exchange, while modelling of cod larvae versus rotifer I levels suggests that optimum I levels in rotifers for cod larvae is 3.5 mg I kg-1 DW.

Highlights

Iodine (I) is essential for vertebrates where it is utilised by the thyroid follicles to produce I containing thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3) (Sutija & Joss, 2005)
Counter to the original hypothesis, we found that cod larvae fed rotifers enriched to copepod levels of iodine displayed symptoms of iodine toxicity
In contrast to the hypothesis, the increased thyroid follicle colloid to epithelium (C/E) ratio observed in this study indicates that I toxicity occurred in cod larvae fed rotifers with 129 mg I kg−1 DW

Summary

Introduction

Iodine (I) is essential for vertebrates where it is utilised by the thyroid follicles to produce I containing thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3) (Sutija & Joss, 2005). Iodine deficiency can lead to thyroid enlargement, termed goitre (Beckett et al, 1993; Vanderpas, 2006; Maier et al, 2007), and alter circulating thyroid hormone levels and ratios (Ruz et al, 1999) These changes are regarded as part of a compensation mechanism. Excessive I intake can negatively affect thyroid hormone production and produce goitre, termed I or colloid goitre (Vanderpas, 2006; Xu et al, 2006; Yang et al, 2006; Franke et al, 2008). This effect is called the Wolff–Chaikoff phenomenom (Wolff & Chaikoff, 1948) and probably occurs because concentrations of iodinated lipids in thyroid follicles increases linearly with available I (Pereira et al, 1990), and these iodinated lipids can inhibit the H2O2 production required for thyroid hormone synthesis (Ohayon et al, 1994; Panneels et al, 1994)

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