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Rotenone is an odorless, colorless, . 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 . 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 , but its use as an insecticide has been banned in many countries.


Discovery
The earliest written record of the now-known rotenone-containing plants used for killing leaf-eating was in 1848; for centuries, these same plants had been used to . The active chemical component was first isolated in 1895 by a French botanist, Emmanuel Geoffroy, who called it nicouline, from a specimen of nicou, now called , while traveling in . He wrote about this research in his thesis, published in 1895 after his death from a parasitic disease. In 1902 , Japanese chemical engineer of the Government-General of Taiwan, isolated a pure crystalline compound from which he called rotenone, after the Taiwanese name of the plant 蘆藤 () translated into Japanese 3=rōten. By 1930, nicouline and rotenone were established to be chemically the same.


Uses

Use as piscicide in fisheries management
When absorbed through the gills, rotenone disrupts cellular respiration in fish, and may lead to their death, depending on the concentration used. Due to this, it has become a key tool in managing ecosystems affected by invasive or unwanted fish species, and as of 2024 there are no viable options that can replace its versatile value in fish removal actions.

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 family, , 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 (days) and is gone from rivers in the course of days and from lakes within a few months, depending on (seasonal) stirring, content, availability of sunlight and temperature.

(2025). 9781934874493, American Fisheries Society.
Rotenone has been used by government agencies to kill fish in rivers and lakes in the United States since 1952, and in Canada and Norway
(2025). 9788242649508, Norsk institutt for naturforskning, NINA rapport.
since the 1980s. It is less frequently used in EU countries, due to strict regulations, but has seen some use in selected countries such as the UK (), Sweden ( and ), Spain (, ) and Hungary ().

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 degradation and ecosystem impact
Rotenone primarily affects gilled organisms such as fish and aquatic invertebrates. Terrestrial animals such as birds, mammals, and amphibians (except tadpoles/larvae) are much less affected by rotenone. When applied in freshwater systems, the treatment dose kills the target fish and usually other gilled species like tadpoles and zooplankton are affected, depending on dosage. However, timing treatments in the fall or winter, when many species are less active, can reduce these impacts. Some taxa may also recover through natural life cycles, such as resting eggs. Its use is more benign for the environment (as compared to drying ponds, or using other piscicides), and studies show that most ecosystems naturally recover within one or two years after rotenone application- with aquatic invertebrates repopulating affected areas,
(2025). 9788232662708, Doctoral theses at NTNU.
thus restoring initial local biodiversity to its status prior to the introduction of the invasive species.

Rotenone decays through and its final product is reduced to and . 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.


Notable administrations as piscicide
Norwegian authorities have been using rotenone since the mid-1980s to eradicate the salmon fluke Gyrodactylus salaris, and as of 2024 48 out of 54 affected river catchments have been treated. Additionally, many lakes and ponds have been rotenone treated in an effort to remove national or regional invasive species, such as , , , , and .Bardal, H. 2019. Small- and large-scale eradication of invasive fish and fish parasites in freshwater systems in Norway. In: C.R. Veitch, M.N. Clout, A.R. Martin, J.C. Russell, and C.J. West (eds.). Island invasives: scaling up to meet the challenge, pp. 457-451. Occasional paper SSC no. 62. Gland, Switzerland: IUCN.

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 ; the cichlids had already spread throughout the and its connected , and by 1994, jaguar cichlids had successfully established themselves throughout and .

In September 2010, Oregon Department of Fish and Wildlife officials used rotenone to kill an established population of present in eastern Oregon's , 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, , 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 , which were probably introduced accidentally by who used them as live bait. The lake was restocked with 20,000 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.


Deactivation
Rotenone can be deactivated in water with the use of potassium permanganate to lower toxicity to acceptable levels.


Use as insecticide
Rotenone was commercialized as cubé, , in single preparation or in combination with other insecticides.
(1991). 9780123341617, . .
It has high acute toxicity to mammals, and all insecticidal uses were banned in the United States and Canada, Re-evaluation Note: Rotenone (REV2008-01, 29 January 2008), Consumer Product Safety, Health Canada in the EU, in the UK, and in Switzerland. It remains legal as a pesticide in a number of other countries, including Australia and New Zealand; the status and effective date of ban in select countries is provided in the table below.

+ Legal status of rotenone as a pesticide, by country
-
31 December 2012
10 October 2008
-
1 January 2014
10 October 2008
23 March 2011 (EPA); 28 January 2019 (USDA)

Rotenone was used in powdered form to treat and on humans, and on , , and 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


Mechanism of action
Rotenone works by interfering with the electron transport chain within complex I in , which places it in IRAC MoA class 21 (by itself in 21B). It inhibits the transfer of electrons from iron-sulfur centers in to . This interferes with NADH during the creation of usable cellular energy (ATP). Complex I is unable to pass off its electron to , creating a back-up of electrons within the mitochondrial matrix. Cellular oxygen is reduced to the radical, creating reactive oxygen species, which can damage and other components of the mitochondria.

Rotenone is used in biomedical research to study the oxygen consumption rate of cells, usually in combination with (an electron transport chain Complex III inhibitor), (an ATP synthase inhibitor) and FCCP (a mitochondrial ).

Rotenone also inhibits assembly.


Presence in plants
Rotenone is produced by extraction from the roots and stems of several tropical and subtropical plant species, especially those belonging to the genera and .

Some of the plants containing rotenone:

  • Hoary pea or goat's rue ( Tephrosia virginiana) – North America
  • Jícama ( Pachyrhizus erosus) – North America
  • Cubé plant or lancepod ( Lonchocarpus utilis) – South America
    • The root extract is referred to as cubé resin
  • Barbasco ( Lonchocarpus urucu) – South America
    • The root extract is referred to as cubé resin
  • Tuba plant ( ) – southeast Asia and southwest Pacific islands
    • The root extract is referred to as derris or derris root
  • Jewel vine ( ) – southeast Asia and southwest Pacific islands
    • The root extract is referred to as derris or derris root
  • Common Mullein ( Verbascum thapsus L.)
  • Cork-bush ( ) – southern Africa
    (2025). 9780869770818, .
  • Florida fishpoison tree ( Piscidia piscipula) – southern Florida, CaribbeanNellis, David N. (1994). Seashore plants of South Florida and the Caribbean. Pineapple Press. 160 p.
  • Several species of and in
    (1999). 9780080912837, . .


Mammalian toxicity
Rotenone is classified by the World Health Organization as moderately hazardous.
(2025). 9789241546638, World Health Organization. .
It is mildly toxic to and other , but extremely toxic to insects and aquatic life, including fish. This higher toxicity in fish and insects is because the rotenone is easily taken up through the or trachea, but not as easily through the skin or the gastrointestinal tract. Rotenone is toxic to .

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 ; 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.


Parkinson's disease
In 2000, injecting rotenone into rats was reported to cause the development of symptoms similar to those of Parkinson's disease (PD). Rotenone was continuously applied over a period of five weeks, mixed with DMSO and PEG to enhance tissue penetration, and injected into the . The study does not directly suggest rotenone exposure is responsible for PD in humans, but is consistent with the belief that to environmental toxins increases the likelihood of the disease. Summary of the article by Dr. Greenamyre on pesticides and Parkinson's Disease at ninds.nih.gov In 2011, a US National Institutes of Health study showed a link between rotenone use and Parkinson's disease in farm workers, suggesting a link between neural damage and pulmonary uptake by not using . Exposure to the chemical in the field can be avoided by wearing a gas mask with filter, which is standard HSE procedure in modern application of the chemical.

Studies with primary cultures of rat and have shown low doses of rotenone (below 10 nM) induce oxidative damage and death of , and it is these neurons in the 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 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 . Further studies involving MPTP have failed to show development of , 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 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.


See also


External links

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