The present bi-partite work describes the development and validation of a mechanistic kinetic model of SODIS E. coli inactivation, enhanced with H2O2. In this first part, the mechanism of the baseline dark phenomena is modelled. A mechanistic model involving E. coli cellular respiration, inactivation due to HO center dot and O-2(center dot-) radicals, and bacterial thermal inactivation, was developed using a series-event model based on the accumulation of damage and cell recovery corrected with the Arrhenius equation for inclusion of the thermal events. The contribution of external H(2)O(2)was included in the internal H2O2 balance, while the balance of extracellular H2O2 considered the consumption caused by its self-decomposition, interactions with cells' membrane, and organic matter from dead cells. Specifically, the kinetic parameters of the external H2O2 sinks, the oxidation reaction of intracellular Fenton, and bacterial thermal inactivation were independently estimated by model regression from experimental data of E. coli inactivation and H2O2 consumption at different controlled conditions of temperature and initial H(2)O(2 )concentration. We complemented the values of the kinetic constants available in the literature with the unknown kinetic parameters estimated from experiemetnal and literature data. The missing kinetic parameters were successfully validated (bacteria error = 4.5%, H2O2 error = 12.9%). This kinetic model helps to understand the intracellular mechanisms and the contributions of each source of inactivation, with the role of radicals' damage being most important at temperatures below 40 degrees C, and the thermal inactivation for temperatures above this value.