Cobalt and Nickel show increasing pollution in our environment. We analyzed their combined toxicity and uptake mechanisms in the early food chain by investigation of bacteria and the ciliate Paramecium as a primary consumer. Exposing Paramecium to metals, we can dissect between phagocytotic uptake and phagocytosis independent uptake. Measurement of cellular content in bacteria after exposure shows a bias for Nickel when both are co-exposed and even increased levels in comparison to single exposure. Imitating the initial food chain, we fed these bacteria to paramecia measuring only phagocytotic uptake. The cellular content shows a similar ratio of Nickel and Cobalt as in food bacteria suggesting that bacteria can selectively pre-accumulate metals for introduction into the food-chain. Analyzing the transcriptomic response of paramecia to sublethal doses of Nickel and Cobalt, Gene ontogogy (GO)-analysis indicates common deregulated pathways, e.g. the ammonium-transmembrane transport and ubiquitine-associated protein degradation. Redox related genes show a massive de-regulation of gene expression indicating cellular adaptation to increased ROS stress. As this suggests that both metals can target also the same cellular pathways, this is in agreement with increased toxicity of both metals in joint applications. Our data reveals complex routes of individual metals to enter the food chain.