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Oceans are warming and pH levels are decreasing as a consequence of increasing levels of dissolved CO2concentrations. The CO2emissions are predicted to be produce in greater and faster changes in the ocean than any other event in geological and historical records over the past 300 million years. Marine organisms will need to respond to multiple stressors but the potential consequences of global change-related effects in fish are not fully understood. Since fish are affected by many biotic and abiotic environmental variables, including temperature and CO2fluctuations, it is critical to investigate how these variables may affect physiological and biochemical processes. We investigated the effects of elevated CO2levels (pH of 8.0, which served as a control, or 7.6, which is predicted for the year 2100) combined with exposure to different temperatures (5, 10, 12, 14, 16, and 18 °C) in the Atlantic halibut (Hippoglossus hippoglossus) during a three month experiment. We assessed effects on antioxidant and cholinesterase enzymes (AChE and BChE), and CYP1A enzyme activities (EROD). The treatments resulted in oxidative stress, and damage was evident in the form of protein carbonyls which were consistently higher in the elevated CO2-treated fish at all temperatures. Analyses of antioxidant enzymes did not show the same results, suggesting that the exposure to elevated CO2increased ROS formation but not defences. The antioxidant defence system was insufficient, and the resulting oxidative damage could impact physiological function of the halibut on a cellular level.

Convergent evidence associates endocrine disrupting chemicals (EDCs) with major, increasingly-prevalent human disorders. Regulation requires elucidation of EDC-triggered molecular events causally linked to adverse health outcomes, but two factors limit their identification. First, experiments frequently use individual chemicals, whereas real life entails simultaneous exposure to multiple EDCs. Second, population-based and experimental studies are seldom integrated. This drawback was exacerbated until recently by lack of physiopathologically meaningful human experimental systems that link epidemiological data with results from model organisms.We developed a novel approach, integrating epidemiological with experimental evidence. Starting from 1,874 mother-child pairs we identified mixtures of chemicals, measured during early pregnancy, associated with language delay or low-birth weight in offspring. These mixtures were then tested on multiple complementary in vitro and in vivo models. We demonstrate that each EDC mixture, at levels found in pregnant women, disrupts hormone-regulated and disease-relevant gene regulatory networks at both the cellular and organismal scale.