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Rotenone is a neurotoxin derived from Derris roots or yam bean of genus Derris or Lonchocarpus It is known to cause Parkinson-like symptoms and is a potent electron transport inhibitor. Rotenone was detected in postmortem specimens in a fatal case of rotenone poisoning with an organic pesticide by liquid chromatography-tandem mass spectrometry with an information-dependent acquisition and MS-MS library search. The forensic specimens were prepared by solid-phase extraction with a Bond Elut(®) Certify cartridge. The mobile phase comprised 5 mM ammonium formate in 10% methanol and 5 mM ammonium formate in 90% methanol. The assay was linear over the range from 0.01 to 1.0 mg/L (r(2) = 0.995). The limit of detection and quantitation in the blood were 0.001 mg/L (signal-to-noise, S/N = 3) and 0.003 mg/L (S/N = 10), respectively. The intraday accuracy and precision for rotenone that were determined by five replicates at 0.02, 0.10 and 1.0 mg/L in blood were <15.0% of bias and <9.0% of CV, respectively. The interday accuracy and precision for rotenone that were determined by seven replicates at 0.02, 0.10 and 1.0 mg/L in blood were <18.0% of bias and <17.0% of CV, respectively. Relative recovery with 0.02, 0.1 and 1.0 mg/L in blood was 104.2, 103.3 and 81.6% (n = 6), respectively. The described method was applied for the determination of rotenone in a fatal case of intoxication of a 33-year-old man who was found dead on a bed in a temporary house. In this case study, the concentrations of rotenone in heart blood (HB), peripheral blood (PB), gastric contents and vitreous humor were 0.77 mg/L, 0.02 mg/L, 126.4 mg/kg and 0.003 mg/L, respectively. The rotenone concentration ratio of the HB/PB was 38.8 and that of gastric contents/PB was 6412.3, suggesting a massive ingestion of rotenone with postmortem redistribution. This study is the report of rotenone detection in a fatal case with the ingestion of the organic insecticide containing rotenone.

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Parkinson disease (PD), the most common neurodegenerative movement disorder, is associated with selective degeneration of nigrostriatal dopamine neurons. Although the underlying mechanisms contributing to neurodegeneration in PD seem to be multifactorial, mitochondrial impairment and oxidative stress are widely considered to be central to many forms of the disease. Whether oxidative stress is a cause or a consequence of dopaminergic death, there is substantial evidence for oxidative stress both in human PD patients and in animal models of PD, especially using rotenone, a complex I inhibitor. There are many indices of oxidative stress, but this review covers the recent evidence for oxidative damage to nucleic acids, lipids, and proteins in both the brain and the peripheral tissues in human PD and in the rotenone model. Limitations of the existing literature and future perspectives are discussed. Understanding how each particular macromolecule is damaged by oxidative stress and the interplay of secondary damage to other biomolecules may help us design better targets for the treatment of PD.

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Rotenone is a pesticide and a piscicide derived from the derris root. The mechanism for the cytotoxicity is at mitochondrial level affecting cellular respiration. A suicide by rotenone poisoning in an adult is described. An innovative laboratory methodology was developed for the principal requirement of the Coroner to determine a positive or negative result to assist in the investigation of the death. The antemortem concentrations detected were 4.05 ng/ml [0.00405 ppm] in the blood and 0.55 ng/ml [0.00055 ppm] in the serum. Toxicity in human is rare and therefore the interpretation of the toxicology results is complicated by the unavailability of a data bank. The cause of death was attributed to rotenone toxicity based on the circumstantial evidence and expert pathological opinion on a balance of probability acceptable under the Coroners Act 1988 and Coroners Rules 1984 in England and Wales. The forensic clinicopathology of rotenone toxicity is discussed.

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INTRODUCTION: Several species of plants in the Fabaceae family are traditionally used for poison fishing because they contain ichthyotoxic rotenoids. In French Guiana two species of Fabaceae belonging to Lonchocarpus genus with a toxic rotenone effect are used for such ancestral practices. Rotenone is of low toxicity for humans when it is diluted, but its neurotoxicity at higher concentrations is well known to users. CASE REPORT: The purpose of this article is to describe a case of self-poisoning by an 86-year-old woman who ingested a bowl of mashed ichthyotoxic plants. Despite early onset of severe symptoms, the patient regained consciousness and resumed normal breathing within a few hours with only symptomatic treatment. CONCLUSION: The clinical pattern observed in this patient (onset of digestive manifestations followed quickly by loss of conscience and respiratory insufficiency) is in agreement with the few poisonings reported in the literature involving other Fabaceae species containing rotenoids in Asia or involving concentrated rotenone used in insecticides. In patients, who survive the initial phase, symptoms usually regress quickly.

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The first fatal case of Yam bean and Rotenone toxicity in Thailand was studied at Forensic Medicine, Chiang Mai, Thailand. A Chinese Taiwan man, 59 years old, was found dead after Yam bean ingestion. Yam bean toxicity and death have been found very rarely in the world and has not been reported in Thailand The Yam bean plant is grown widely in Northern Thailand. But many people know that mature pods, seeds and filage of the Yam bean, except the tuberous root, are very toxic. The victim ate a lot of Yam bean seeds and died within 2 hours with respiratory failure. The authors detected Rotenone substance in Yam bean seeds, gastric content and 72 ng/ml blood by HPLC. Also generalized microscopic hemorrhage in the brain, lungs, liver and adrenal glands which were of characteristic pathology were detected. The authors concluded that the cause of death was asphyxia from Yam bean or Rotenone toxicity.

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Rotenone is a pesticide derived from the roots of plants from the Leguminosae family. Poisoning following deliberate ingestion of these plant roots has commonly been reported in Papua New Guinea. However, poisoning with commercially available rotenone in humans has been reported only once previously following accidental ingestion in a 3.5-year-old child. Therefore, the optimal management of rotenone poisoning is not known. After deliberate ingestion of up to 200 ml of a commercially available 0.8% rotenone solution, a 47-year-old female on regular metformin presented with a reduced level of consciousness, metabolic acidosis and respiratory compromise. Metformin was not detected in premortem blood samples obtained. Despite intensive supportive management, admission to an intensive care unit, and empirical use of N-acetylcysteine and antioxidant therapy, she did not survive. Poisoning with rotenone is uncommon but is potentially fatal because this agent inhibits the mitochondrial respiratory chain. In vitro cell studies have shown that rotenone-induced toxicity is reduced by the use of N-acetylcysteine, antioxidants and potassium channel openers. However, no animal studies have been reported that confirm these findings, and there are no previous reports of attempted use of these agents in patients with acute rotenone-induced toxicity.

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Rotenone-poisoned rat liver mitochondria energized by succinate addition, after a 5-min period of preincubation in presence of 10 microM Ca2+, produce H2O2 at much faster rates, undergo extensive swelling, and are not able to retain the membrane potential and accumulated Ca2+. Similar results were obtained when a suspension of rat liver mitochondria preincubated in anaerobic medium for 5 min was reoxygenated. The addition of either ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, ruthenium red, catalase, or dithiothreitol, just before succinate or O2 addition, prevented mitochondrial swelling, indicating the involvement of Ca2+, reactive oxygen species, and oxidation of membrane protein thiols in this process of membrane permeabilization. Inhibition of mitochondrial swelling by cyclosporin A suggests that the membrane alterations observed under these experimental conditions are related to opening of the permeability transition pore. The presence of carbonyl cyanide p-trifluoromethoxyphenylhydrazone, which prevents Ca2+ cycling across the membrane, did not inhibit mitochondrial swelling when Ca2+ influx into the mitochondrial matrix was driven by a high Ca2+ gradient. When rotenone plus antimycin A-poisoned mitochondria were energized by N,N,N',N'-tetramethyl-p-phenylenediamine, which reduces respiratory chain complex IV, mitochondrial swelling did not occur, unless succinate, which reduces coenzyme Q, was also added. It is concluded that reduced coenzyme Q is the electron source for oxygen radical production during Ca(2+)-stimulated oxidative damage of mitochondria.

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A case of a fatal rotenone poisoning in a three-and-a-half-year-old girl is described. The case report and autopsy findings are mentioned. For the extraction of rotenone out of biological samples, a solvent partitioning and silica gel open column chromatographic cleanup procedure has been used. The determination of rotenone was performed by high pressure liquid chromatography.

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