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Rotenone: Carcinogenic Potency Database potency.berkeley.edu |
Rotenone is an odorless chemical that is used as a broad-spectrum insecticide, piscicide, and pesticide. It occurs naturally in the roots and stems of several plants such as the jicama vine plant. It causes Parkinson's disease-like symptoms if injected into rats. Rotenone kills the freshwater snail Lymnaea stagnalis by attacking the mitochondria in its neurons.[citation needed]
[edit] HistoryEmmanuel Geoffroy first isolated rotenone from a specimen of Robinia nicou, now called Lonchocarpus nicou, while traveling in French Guiana.[1] He wrote about this research in his thesis, published posthumously in 1895 after his death from a parasitic disease.[2] Researchers later determined that the substance which Geoffroy termed nicouline was identically rotenone. [edit] UsesRotenone is used in solution as a pesticide and insecticide. It is commonly used in powdered or emulsified liquid form in fisheries management to remove unwanted fish species,[3] such as the eradication of exotic fish from non-native habitats. People catch fish by extracting rotenone from plants and releasing it into water. Poisoned fish come to the surface and are easily caught. This method was first practiced by various indigenous tribes[4] who smashed the roots. Fish caught this way can be eaten because rotenone is very poorly absorbed by the gastrointestinal tract of humans, whereas it is lethal to fish because it readily enters the blood stream of the fish through the gills. Small-scale sampling with rotenone is used by fish researchers studying the biodiversity of marine fishes to collect cryptic, or hidden, fishes, which represent an important component of shoreline fish communities. Rotenone is the most effective tool available because only small quantities are necessary. It has only minor and transient environmental side-effects.[5] Rotenone is also used in powdered form to reduce parasitic mites on chickens and other fowl. In the United States and in Canada, all uses of rotenone except as a piscicide (fish killer) are being phased out.[6][7] [edit] Method of actionRotenone works by interfering with the electron transport chain in mitochondria. Specifically, it inhibits the transfer of electrons from iron-sulfur centers in complex I to ubiquinone. This prevents NADH from being converted into usable cellular energy (ATP). [edit] Presence in plantsRotenone is produced by extraction from the roots and stems of several tropical and subtropical plant species, especially those belonging to the genus Lonchocarpus or Derris. Some of the plants containing rotenone:
[edit] ToxicityRotenone is classified by the World Health Organization as moderately hazardous.[11] It is mildly toxic to humans and other mammals, but extremely toxic to insects and aquatic life including fish. This higher toxicity in fish and insects is due to the fact that the lipophilic rotenone is easily taken up through the gills or trachea, but not as easily through the skin or through the gastrointestinal tract. The lowest lethal dose for a child is 143 mg/kg. Human deaths attributed to Rotenone are rare because its irritating action causes vomiting.[12] Deliberate ingestion of rotenone can be fatal.[13] The compound breaks down when exposed to sunlight and usually has a short lifetime of six days in the environment.[14] In water rotenone may last six months.[citation needed] Rotenone is classified by the USDA National Organic Program as a nonsynthetic and was allowed to be used to grow "organic" produce until 2005 when it was removed from the list of approved substances due to concerns about its safety.[15] [edit] Parkinson's diseaseIn 2000 it was reported that injecting rotenone into rats causes symptoms of Parkinson's disease to develop. Rotenone was continuously applied over a period of five weeks, mixed with DMSO and PEG to enhance tissue penetration, and injected into the jugular vein.[16] The study does not directly suggest that rotenone exposure is responsible for Parkinson's disease in humans but is consistent with the belief that chronic exposure to environmental toxins increases the likelihood of the disease.[17] In addition, studies with primary cultures of rat neurons and microglia have shown low doses of rotenone (below 10 nM) to induce oxidative damage and death of dopaminergic neurons[18] and it is these neurons in the substantia nigra that die in Parkinson's disease. It had been known earlier that the neurotoxin MPTP causes Parkinson's symptomatology (in humans and other primates, though not in rats) by interfering with Complex I in the electron transport chain and killing dopaminergic neurons in the substantia nigra. However, further studies involving MPTP have failed to show development of Lewy bodies, a key component to Parkinson's pathology. Therefore, the mechanism behind MPTP as it relates to Parkinson's Disease is not fully understood.[19] Because of these developments, rotenone was investigated as a possible Parkinson-causing agent. Both MPTP and rotenone are lipophilic and can cross the blood-brain barrier. [edit] See also[edit] References
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