Hypochlorous acid, HOCl, is one of the most powerful biological oxidants and the most important mediator of inflammatory damage of cells and tissues. The purpose of this study was to characterize the morphological features of HOCl – induced oxidative impairment in rat liver mitochondria in vitro and to compare the processes of HOCl-induced oxidation in mitochondria, erythrocytes and B14 cells.HOCl addition (300 μM) to mitochondrial suspension resulted in mitochondrial structural changes with a decrease in the mean total length of the crista and the average number of cristae in one mitochondria with no change in the length of one crista. There was shown a slight decrease in the average cross-sectional area of one mitochondria, mitochondrial profile elongation, an increase in the number of altered mitochondria and the heterogeneity of the population. Simultaneously we observed depolarization of the mitochondrial membrane, the rate and degree of which were determined by the concentration of HOCl. HOCl addition (25–150 μМ) induced lysis of erythrocytes for 60–180 s, which was preceded by a change in the shape and size of cells. The apparent dissociation constant for the HOCl – membrane complex was estimated to be Kd = 140 ± 25 μМ, and the Hill coefficient was to be 2.1. The B14 cell exposure to HOCl (100 μМ) led to a loss of ability to sorb on the substrate, to form associates, and to subsequent shrinkage of cells.Therefore, HOCl caused some morphological (and functional) changes in rat liver mitochondria, which may serve as one of the causes of cell death in inflammatory foci. At the level of the whole cells, the HOCl addition induced lysis of red blood cells and deep damage to B14 cells.
Biochemical and morphological changes in isolated rat liver mitochondria exposed to ultraviolet light.
