Fig. 2
From: Embryo development is impaired by sperm mitochondrial-derived ROS
Effect of cyanide on mitochondrial-derived ROS. (A) Schematic representation of the mechanisms by which cyanide disrupts the mitochondrial electron transport chain. Under physiological conditions, respiratory complexes I, II and III leak electrons to oxygen producing the superoxide anion (O2●−), which can be later converted into reactive oxygen species (ROS) [18]. In the presence of cyanide, the heme a3-CuB binuclear centre of Complex IV is blocked [32], thus preventing electrons from reaching molecular oxygen and inhibiting the electron transport chain [18]. Not only does this inhibition prevent the formation of O2●− and derived ROS products along the electron transport chain, but it also reduces MMP and OCR. (B) Effect of cyanide (5 mM and 10 mM) on sperm viability, sperm motility, MMP, OCR, and intracellular levels of total ROS and superoxides (O2●−). Cyanide treatments were normalised to the control in each biological replicate (n = 12). Data are represented as mean ± standard error of the mean. Significant differences (P < 0.05) are marked with *. OCR: oxygen consumption rate. MMP: mitochondrial membrane potential. ROS: reactive oxygen species