Important in the process of apoptosis, caspases are a family of proteases that mediate cell death. In particular, caspase-3 plays a central role in the apoptotic signalling network and leads to DNA fragmentation and the cell��s demise. Casp-3 and GST may represent early physiological responses for the mitigation of the detrimental effects of UVR and that could complement other UVR defences acting at longer time scales. In addition to DNA damage, UVR can cause carboxylation of proteins and peroxidation of lipids, and detrimental effects on physiological endpoints as respiration rates and neurological dysfunctions like alterations in cholinesterase activity, among others. Hence, we include ChE activity as sensor of Butylhydroxyanisole cellular damage in relation with the balance of protective systems of GST and Casp-3. It is well known how organisms handle UVR Ganciclovir threat that fluctuates over the long term, for example by accumulating photoprotective compounds, but the knowledge of responses at the cellular level to short term UVR threats is negligible. A rapid enzymatic response to handle fluctuations in UVR may be extremely important for the performance of the organism. But all protective responses that involve phenotypic plasticity, such as in UVR protection, must undergo an initial time lag before they become effective, however this time-lag will vary greatly depending on the mechanism involved. Thus, we hypothesize that enzymatic responses to UVR stress will act on short time scales, and that these responses vary according to the developmental stage of the organism. In order to test these hypotheses, a laboratory study was designed to assess the balance among different enzymes linked to important protective mechanisms, namely GST and Casp-3, as fast and coordinated responses to UVR in two different developmental stages of the calanoid copepod Eudiaptomus gracilis. We provide the first evidence on how UVR affects Casp-3, as well as the interplay with other enzyme protective systems as GST. When intermittent environmental threats are part of an organism��s existence, the defence that they mount may be either constitutive and permanent or inducible and temporary. For these latter plastic responses, a lag phase of variable length is necessarily entailed, which means that during this phase the organism is relatively unprotected against the threat. Defences against UVR damage, such as pigments and other photoprotective compounds, are quite well known. Yet studies focusing on short-term boosts of UVR exposure, and the sublethal effects of such, are surprisingly rare, even though such fluctuations occur regularly in nature, e.g. due to daily changes in weather conditions and clouding. Here we show, for the first time, how short-term UVR exposure at similar to natural, sub-lethal levels simultaneously triggers responses in two different enzyme systems involved in key cellular processes.