Previous studies on mycobacterial respiratory pathways have been published. Ortega-Calvo and Gschwend reported that sorption to sediment black carbon resulted in oxygen limitation for aerobic Polycyclic Aromatic Hydrocarbon biodegradation. Furthermore,LP117 Fritzsche reported that pyrene degradation at low oxygen concentrations does not produce any additional metabolites or intermediates which might be expected as the result of the activity of an oxygenase with low oxygen affinity, such as aromatic ring cleavage monooxygenases. With the high affinity of the aromatic ring cleavage dioxygenases for molecular oxygen, there is the possibility of more oxygen being diverted for dioxygenase activity as compared to cytochrome oxidase activity. The aim of the present investigation was to determine the molecular basis of this shift in respiration based on the expression of various respiratory enzyme components measured in a constantly aerated culture medium. Microbial growth requires the biosynthesis of a specific range of monomers which are assembled into polymers to form the bulk of new biomass. Microorganisms aerobically take up different carbon compounds as carbon and energy sources, and degrade them into intermediates which are then utilized in the central FINDY metabolic pathway. Energy production in a living cell is intertwined with these metabolic processes as they require the input of energy and precursors in various forms. In aerobic respiration when glucose is available as a substrate, most of the free energy released during the oxidation of glucose to CO2 is retained in the reduced coenzymes NADH and FADH2 which are generated during glycolysis and the citric acid cycle. The use of FADH2 in energy production is considered a common pathway for energy metabolism in adaptation to hypoxic environments in bacteria. FADH2 is transferred to a low potential quinone, such as naphthoquinone, by complex I and is finally oxidized by the fumarate reductase activity of complex II which is a reverse reaction of the succinate– ubiquinone reductase activity of complex II.