So the next logical question is why rotenone is only toxic to certain organisms, mainly fish and insects. The pesticide rotenone specifically inhibits electron transfer early in the chain with inhibition of proton transport beginning at site 1. Rotenone kills fish by inhibiting cellular respiration and the ability to use dis-solved oxygen. So why is rotenone only toxic in this way to fish and insects? Typically, rotenone-containing plants in the legume family, Fabaceae, are crushed and introduced into a body of water, and as rotenone interferes with cellular respiration, the affected fish rise to the surface in an attempt to gulp air, where they are more easily caught. Rotenone is able to inhibit cellular respiration in almost every living organism, including mammals, fish, amphibians, insects and even plants. (1969) concluded that the selective toxicity of fish, Draining and chemical treatment are usually the only practical way to completely eradicate invasive fish. Rotenone has historically been used by indigenous peoples to catch fish. Rotenone generally works by inhibiting cellular respiration in mitochondria (where and how energy is produced). Rotenone is derived from the roots and stems of cer-tain tropical and subtropical plants. Rotenone will remove fish only when the correct concentration is applied. Many chemicals can interfere with cellular respiration by binding to the cytochromes that constitute the electron transport chain and inhibiting the flow of electrons along this protein complex. Rotenone induced a transitory decrease in cellular respiration (0-4 h after treatment). Rotenone kills fish by inhibiting cellular respiration and the ability to use dissolved oxygen. Cell respiration then progressively recovered and reached a steady state at 10 to 12 h after treatment. Complex I inhibition by rotenone did not induce obvious oxidative stress or cell death but affected longer term cell growth. Fish are highly susceptible because rotenone can efficiently and quickly enter the blood stream through the gills. Effect of vehicle (control, open triangle) or acetaminophen (10 mM, green triangle) on (b) routine respiration supported by endogenous substrates and (c) complex II-linked respiration in the presence of rotenone and the cell-permeable succinate prodrug NV241 in intact human platelets. In effect, the fish suffocate. Fish are highly susceptible because rotenone can efficiently and … Rotenone has the ability to inhibit cellular respiration in almost every living organism, including mammals, fish, amphibians, insects, and even plants (Bradbury 1986). This leads to reduced cellular uptake of oxygen and eventual cell death. Rotenone is derived from roots and stems of certain tropical and subtropical plants. Readily absorbed through the gills, rotenone is lethal to fish because it blocks the biochemical process that allows fish to utilize the oxygen in their blood during cellular respiration. Data are expressed as individual scatter plots, mean and range. Rotenone is able to inhibit cellular respiration in almost every living organism, including mammals, fish, amphibians, insects and even plants. So why is rotenone only toxic in this way to fish and insects? Fish are particularly sensitive to rotenone because the chemical easily enters their blood stream directly through their gills. Exposure of the neuronal-originating SH-SY5Y cells to very low dose (10 pM) rotenone, a mitochondrial-respiration complex (Co)I inhibitor, for 72 or 96 h did not affect cell viability and reactive oxygen species (ROS) levels. Fish exposed to lethal rotenone concentrations move to the surface and gasp for oxygen as if the water was oxygen-depleted. Specifically, inhibition of cellular respiration by rotenone results in the compensatory induction of glycolysis, loss of bioenergetic reserve capacity, activation of the apoptotic cascade and a strong correspondence between the doses which cause bioenergetic dysfunction and cell death. Fukami et al. Rotenone is a natural compound that has been used to interfere with mitochondrial respiration, in particular with Complex I activity, and hence to reduce intracellular ATP levels especially in OXPHOS-dependent cell lines [25, 26].
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