Abstract
•Iron nanoparticles are widely used in all life domains but might be toxic.•Despite its importance, mitochondrial toxicity is poorly known.•Brain, heart, lung, liver and kidneys were submitted to Fe3O4 nanoparticles.•Mitochondrial coupling and respiratory chain complexes were not impaired.•Iron nanoparticles did not show mitochondrial toxicity in normal rats.
The present study evaluates the effects of iron oxide nanoparticles (ION) on mitochondrial respiratory chain complexes activities in five organs characterized by different oxidative capacities and strongly involved in body detoxification. Isolated mitochondria were extracted from brain, heart, lung, liver and kidneys in twelve Wistar rats (8weeks) using differential centrifugations. Maximal oxidative capacities (Vmax), mitochondrial respiratory chain complexes activity using succinate (Vsucc, complexes II, III, and IV activities) or N, N, N′, N′-tetramethyl-p-phenylenediaminedihydrochloride (tmpd)/ascorbate (Vtmpd, complex IV activity) and, mitochondrial coupling (Vmax/Vo) were determined in controls and after exposure to 100, 200, 300 and 500μg/ml Fe3O4. Data showed that baseline maximal oxidative capacities were 26.3±4.7, 48.9±4.6, 11.3±1.3, 27.0±2.5 and 13.4±1.7μmol O2/min/g protein in brain, heart, lung, liver, and kidneys mitochondria, respectively. Complexes II, III, and IV activities also significantly differed between the five organs. Interestingly, as compared to baseline values and in all tissues examined, exposure to ION did not alter mitochondrial respiratory chain complexes activities whatever the nanoparticles (NPs) concentration used. Thus, ION did not show any toxicity on mitochondrial coupling and respiratory chain complexes I, II, III, and IV activities in these five major organs.