In the context of fast-paced global changes, understanding the adaptive potential of organisms to stressors is paramount. This study investigates whether prior stress can alter an individual’s response to mutagens. We hypothesised that this would increase mutation rates, providing scope for rapid adaptation. To explore this, we exposed zebrafish (Danio rerio) embryos to heat stress (up to 32°C) prior to a UVB/UVA damage/repair assay. To account for the complex social propagation of stress in natural environments, we also exposed embryos to social metabolites from stressed conspecifics, in isolation and in combination to heat stress, prior to the UV assay. Our findings reveal a surprising hormetic effect of heat stress that protected and/or rescued embryos from UV damage by activating cellular stress pathways and DNA repair mechanisms. This protective effect improved their overall fitness as the embryos presented less mutations, less defects and performed better in behavioural assays. Whilst not supporting our initial hypothesis, this suggests the potential adaptive significance of stress preconditioning, at least at sublethal levels of stress history. However, when heat stress was coupled with social metabolites, further activation of stress molecular pathways prevented the heat hormetic effect, in turn increasing mutation rates and declining larval performance, emphasising the importance of considering social contexts in stress response studies. Our results demonstrate the complexity of stress responses and the need to consider cross-protective mechanisms but also social stress propagation in predicting the adaptive potential of aquatic animals to global changes.