Rotenone is an odorless, colorless, crystalline isoflavone. It occurs naturally in the seeds and stems of several plants, such as the jicama vine, and in the roots of several other members of the Fabaceae. It was the first-described member of the family of chemical compounds known as . Rotenone is approved for use as a piscicide to remove alien fish species, see Uses. It has also been used as a broad-spectrum insecticide, but its use as an insecticide has been banned in many countries.
Its value in ecosystem restoration is appreciated due to its rapid degradation, when exposed to light and warm temperatures, making it a temporary measure with minimal long-term environmental effects, see Rotenone and Ecosystem Impact.
Rotenone is used as a nonselective piscicide (fish killer). Rotenone has historically been used by indigenous peoples to catch fish. 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, where they are more easily caught.
In modern times it is frequently used as a tool to remove alien fish species, as it has a relatively short half-life (days) and is gone from rivers in the course of days and from lakes within a few months, depending on (seasonal) stirring, Organic matter content, availability of sunlight and temperature.
Rotenone has also seen some use in other field studies in the marine environment needing only small quantities. 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, since it has only minor, local and transient environmental side effects.
Rotenone decays through and its final product is reduced to water and carbon dioxide. It oxidizes to rotenolone, which is about an order of magnitude less toxic than rotenone. In water, the rate of decomposition depends upon several factors, including temperature, pH, water hardness and sunlight. The half-life of rotenone in a pond of 1.1 mean depth ranged from half a day at 24 °C to 3.5 days at 0 °C, but in deeper oligotrophic systems (thus less degradation due to sunlight and organic content) the half-life may be considerably longer.
In 1992, Florida Fish and Wildlife Conservation Commission (FWC) officials used rotenone to eradicate an established population of invasive jaguar cichlids from a small pond in Miami-Dade County. Officials were successful in killing every jaguar cichlid (along with every other fish) in the pond, but unsuccessful in eradicating them from Florida; the cichlids had already spread throughout the Miami Canal and its connected , and by 1994, jaguar cichlids had successfully established themselves throughout Southern Florida and Central Florida.
In September 2010, Oregon Department of Fish and Wildlife officials used rotenone to kill an established population of invasive species goldfish present in eastern Oregon's Mann Lake, with the intention of not disrupting the lake's native Lahontan cutthroat trout population. Rotenone successfully achieved these aims, killing between 179,000–197,000 goldfish and , and only three trout.
Beginning May 1, 2006, Panguitch Lake, a reservoir in the southeastern portion of the U.S. state of Utah, was treated with rotenone, to potentially eradicate and control the invasive population of Utah chub, which were probably introduced accidentally by Fisherman who used them as live bait. The lake was restocked with 20,000 rainbow trout in 2006; as of 2016, the lake's fish population has recovered.
In 2012, rotenone was used to kill all remaining fish in Stormy Lake (Alaska) due to invasive pike destroying native species, which were reintroduced once the treatment was concluded.Earl, Elizabeth, Fish population booms in Stormy Lake Peninsula Clarion, 10/7/2015
In 2014, rotenone was used to kill all remaining fish in San Francisco's Mountain Lake, which is located in Mountain Lake Park, in order to rid it of invasive species introduced since the migration of European settlers to the region.
+ Legal status of rotenone as a pesticide, by country |
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31 December 2012 |
10 October 2008 |
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1 January 2014 |
10 October 2008 |
23 March 2011 (EPA); 28 January 2019 (USDA) |
Rotenone was used in powdered form to treat scabies and head lice on humans, and parasitic on chickens, livestock, and pet animals.
In agriculture it was unselective in action and killed , , , , , and , as well as most other arthropods. It biodegrades rapidly in soil, with 90% degraded after 1–3 months at and three times faster at . The compound decomposes when exposed to sunlight and usually has an activity of six days in the environment.Vitax Safety Data Sheet for Derris dust, revised October 1998
Rotenone is used in biomedical research to study the oxygen consumption rate of cells, usually in combination with antimycin A (an electron transport chain Complex III inhibitor), oligomycin (an ATP synthase inhibitor) and FCCP (a mitochondrial uncoupler).
Rotenone also inhibits microtubule assembly.
Some of the plants containing rotenone:
The lowest lethal dose for a child is not known, but death occurred in a 3.5-year-old child who had ingested 40 mg/kg rotenone solution. Human deaths from rotenone poisoning are rare because its irritating action causes vomiting. Deliberate ingestion of rotenone can be fatal.
A 2018 study, which examined the effects of rotenone administration on cell cultures that mimicked properties of developing brains, found that rotenone may be a developmental neurotoxicant; that is, that rotenone exposure in the developing fetus may impede proper human brain development, with potentially profound consequences later in life. The study found that rotenone was particularly damaging to dopaminergic neurons, consistent with prior findings.
Studies with primary cultures of rat and microglia have shown low doses of rotenone (below 10 nM) induce oxidative damage and death of dopaminergic neurons, and it is these neurons in the substantia nigra that die in Parkinson's disease. Another study has also described toxic action of rotenone at low concentrations (5 nM) in dopaminergic neurons from acute rat brain slices. This toxicity was exacerbated by an additional cell stressor – elevated intracellular calcium concentration – adding support to the 'multiple hit hypothesis' of dopaminergic neuron death.
The neurotoxin MPTP had been known earlier to cause PD-like symptoms (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. Further studies involving MPTP have failed to show development of Lewy bodies, a key component to PD pathology. However at least one study recently has found evidence of protein aggregation of the same chemical makeup as that which makes up Lewy bodies with similar pathology to Parkinson's disease in aged from MPTP. Therefore, the mechanism behind MPTP as it relates to Parkinson's disease is not fully understood. Neurotransmitters and Disorders of the Basal Ganglia -- Basic Neurochemistry -- NCBI Bookshelf, American Society for Neurochemistry 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.
In 2010, a study was published detailing the progression of Parkinson's-like symptoms in mice following chronic intragastric ingestion of low doses of rotenone. The concentrations in the central nervous system were below detectable limits, yet still induced PD pathology.
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