Organ health and development in larval kingfish are unaffected by ocean acidification and warming

PeerJ. 2019 Dec 12:7:e8266. doi: 10.7717/peerj.8266. eCollection 2019.

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.

Keywords: Aquaculture; CO2; Climate change; Commercial fish; Environmental impacts; Histology; Larval development; Seriola lalandi; Temperature; pH.

Grants and funding

Funding was provided by the Government of New Zealand, and Principality of Monaco through the Pacific Islands Ocean Acidification Partnership (PIOAP), The Pacific Community (SPC), Australian Research Council (ARC), Grant/ Award Number: FT130100505, ARC Centre of Excellence for Coral Reef Studies, and the New Zealand’s National Institute of Water and Atmospheric Research (NIWA). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.