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Recent research from our group has highlighted the significance of metabolic priming and the suitability of human dermal fibroblasts (NHDF) as a cell model for mitochondrial and redox theragnostics. However, when delving into the redox reorganization associated with metabolic priming, we encountered a marked variability in cellular responses to oxidant agents like H2O2 and tBHP. In this manuscript, we explore the underlying causes of this variability, including cell population density and cell cycle distribution at the time of the insult, and H2O2 stock solution stability. We observed that the density of cells at the time of oxidant exposure significantly influenced the cellular response, suggesting a density-dependent modulation of stress responses. Changes in cell cycle distribution at the time of oxidative insult were also found to contribute to the observed heterogeneity in cellular responses. Specifically, higher mitochondrial polarization in OX medium was associated with a lower percentage of cells in the G2/M cell cycle phase. Our findings reveal important insights into the interplay between metabolic state, oxidative stress, and cell cycle, which may have implications for understanding disease mechanisms and developing therapeutic strategies. Our goal is to contribute to the improvement of in vitro models for studying oxidative stress that can be used for the development of clinically relevant redox-based therapies.