Background: Cadmium is a widespread contaminant and a recognized carcinogen. We previously showed that the administration of low cadmium doses for 24 hours treatment to healthy C3H10T1/2Cl8 cells at the beginning of Cell Transformation Assay (CTA), up regulates genes involved in metal scavenging and antioxidant defense, like metallothioneines, Glutathione S transferases and heat shock proteins. Still, although most cells thrive normally in the following weeks, malignancy is triggered by cadmium and leads to foci of transformed cells appearance at the end of the CTA. In this work we aim at elucidating the early metabolic deregulation induced by cadmium, underlying healthy cell transformation into malignant cells.Methods: Respiratory metabolism was investigated through Seahorse Agilent assays in different conditions, while oxidative stress level was assessed through fluorescent probes; DNA damage was evaluated by Comet assay and mitochondrial morphology was analyzed in confocal microscopy.Results: Results show that, although initial response to cadmium is effective in balancing oxidative stress, through mitochondria rearrangement, SOD1 activity is inhibited, leading to increased O 2 level, which in turn causes DNA strand breaks. From the metabolic point of view, cells increase their glycolytic flux, although all extra NADH produced is still efficiently reoxidized by mitochondria.Conclusions: Our results confirm previously shown response against cadmium toxicity; new data about glycolytic increase and mitochondrial rearrangements suggest pathways leading to cell transformation.General significance: In this work we exploit the widely used, well known CTA, which allows following healthy cells transformation into a malignant phenotype, to understand early events in cadmiuminduced carcinogenesis.