Abstract
Kelp are main iodine accumulators in the ocean, and their growth and photosynthesis are likely to benefit from elevated seawater CO2 levels due to ocean acidification. However, there are currently no data on the effects of ocean acidification on iodine metabolism in kelp. As key primary producers in coastal ecosystems worldwide, any change in their iodine metabolism caused by climate change will potentially have important consequences for global geochemical cycles of iodine, including iodine levels of coastal food webs that underpin the nutrition of billions of humans around the world. Here, we found that elevated pCO2 enhanced growth and increased iodine accumulation not only in the model kelp Saccharina japonica using both short‐term laboratory experiment and long‐term in situ mesocosms, but also in several other edible and ecologically significant seaweeds using long‐term in situ mesocosms. Transcriptomic and proteomic analysis of S. japonica revealed that most vanadium‐dependent haloperoxidase genes involved in iodine efflux during oxidative stress are down‐regulated under increasing pCO2, suggesting that ocean acidification alleviates oxidative stress in kelp, which might contribute to their enhanced growth. When consumed by abalone (Haliotis discus), elevated iodine concentrations in S. japonica caused increased iodine accumulation in abalone, accompanied by reduced synthesis of thyroid hormones. Thus, our results suggest that kelp will benefit from ocean acidification by a reduction in environmental stress however, iodine levels in kelp‐based coastal food webs will increase, with potential impacts on biogeochemical cycles of iodine in coastal ecosystems.
Original language | English |
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Pages (from-to) | 629-639 |
Number of pages | 11 |
Journal | Global Change Biology |
Volume | 25 |
Issue number | 2 |
Early online date | 8 Oct 2018 |
DOIs | |
Publication status | Published - Feb 2019 |
Keywords
- Saccharina japonica
- iodine metabolism
- kelp
- ocean acidification
- thyroid hormone
- vanadium-dependent haloperoxidase