Abstract
Anthropogenic CO2 emissions are causing global ocean warming and ocean acidification. The early life stages of some marine fish are vulnerable to elevated ocean temperatures and CO2 concentrations, with lowered survival and growth rates most frequently documented. Underlying these effects, damage to different organs has been found as a response to elevated CO2 in larvae of several species of marine fish, yet the combined effects of acidification and warming on organ health are unknown. Yellowtail kingfish, Seriola lalandi, a circumglobal subtropical pelagic fish of high commercial and recreational value, were reared from fertilization under control (21 °C) and elevated (25 °C) temperature conditions fully crossed with control (500 µatm) and elevated (1,000 µatm) pCO2 conditions. Larvae were sampled at 11 days and 21 days post hatch for histological analysis of the eye, gills, gut, liver, pancreas, kidney and liver. Previous work found elevated temperature, but not elevated CO2, significantly reduced larval kingfish survival while increasing growth and developmental rate. The current histological analysis aimed to determine whether there were additional sublethal effects on organ condition and development and whether underlying organ damage could be responsible for the documented effects of temperature on survivorship. While damage to different organs was found in a number of larvae, these effects were not related to temperature and/or CO2 treatment. We conclude that kingfish larvae are generally vulnerable during organogenesis of the digestive system in their early development, but that this will not be exacerbated by near-future ocean warming and acidification.
Highlights
Increasing anthropogenic CO2 emissions to the atmosphere are leading to two major problems for marine ecosystems: rising ocean temperatures (Bindoff et al, 2007) and ocean acidification (OA) (Doney et al, 2009)
Both elevated CO2 and temperature did lead to an increase in resting oxygen uptake relative to the control (Laubenstein et al, 2018). This suggests that larvae were expending more energy at rest in the elevated CO2 and temperature treatments, than the control animals. This is consistent with our liver histology results, where we found a trend towards decreased lipid contents in the elevated CO2 and temperature treatments, indicating that the larvae
Our results suggest that the early life stage around 11 days post hatch is vulnerable for kingfish larvae and leads to considerable variation in organ health among individuals consistent with high mortality rates
Summary
Increasing anthropogenic CO2 emissions to the atmosphere are leading to two major problems for marine ecosystems: rising ocean temperatures (Bindoff et al, 2007) and ocean acidification (OA) (Doney et al, 2009). OA is caused by the uptake of atmospheric CO2 at the ocean surface, where carbon dioxide is converted to bicarbonate, releasing hydrogen ions in the process. This increase in hydrogen ions has lowered the pH of the ocean surface globally by 0.1 pH units since pre-industrial times, with a further decline of 0.2–0.3 pH units predicted to occur within this century (Caldeira & Wickett, 2005). Concurrent to OA, sea surface temperatures have increased globally by about 1 C since pre-industrial times and are predicted to rise 2–4 C by the end of the century due to the enhanced green-house effect of atmospheric CO2 (Collins et al, 2013). Our ability to predict effects and make inferences for communities and ecosystems is limited by inadequate knowledge of the likely impacts of these stressors on important functional groups, such as large pelagic fishes
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