Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin

Smith, Brent E.; Hsu, Walter H.; Yang, Ping-Cheng

doi:10.1007/bf01974698

Cited by 23 publications

(15 citation statements)

References 14 publications

(8 reference statements)

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“…For example, the organotin fentin was identified in ToxCast™ as a target for PPARγ at a relatively low concentration (U.S. EPA 2011a; search for “fentin”). Amitraz, a formamidine insecticide, is an α2-adrenoreceptor agonist (Chen and Hsu 1994; Hugnet et al 1996; Smith et al 1990), and this activity was identified in ToxCast™ (U.S. EPA 2011a; search for “amitraz”).…”

Section: Use Of Tox21 Hts To Identify Substances Of Potential Interestmentioning

confidence: 99%

Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review

Thayer

Heindel²,

Bucher³

et al. 2012

Environ Health Perspect

541

364

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Background: There has been increasing interest in the concept that exposures to environmental chemicals may be contributing factors to the epidemics of diabetes and obesity. On 11–13 January 2011, the National Institute of Environmental Health Sciences (NIEHS) Division of the National Toxicology Program (NTP) organized a workshop to evaluate the current state of the science on these topics of increasing public health concern.Objective: The main objective of the workshop was to develop recommendations for a research agenda after completing a critical analysis of the literature for humans and experimental animals exposed to certain environmental chemicals. The environmental exposures considered at the workshop were arsenic, persistent organic pollutants, maternal smoking/nicotine, organotins, phthalates, bisphenol A, and pesticides. High-throughput screening data from Toxicology in the 21st Century (Tox21) were also considered as a way to evaluate potential cellular pathways and generate -hypotheses for testing which and how certain chemicals might perturb biological processes related to diabetes and obesity.Conclusions: Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life. Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap. In this workshop review, we outline the major themes that emerged from the workshop and discuss activities that NIEHS/NTP is undertaking to address research recommendations. This review also serves as an introduction to an upcoming series of articles that review the literature regarding specific exposures and outcomes in more detail.

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Section: Use Of Tox21 Hts To Identify Substances Of Potential Interestmentioning

confidence: 99%

Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review

Thayer

Heindel²,

Bucher³

et al. 2012

Environ Health Perspect

541

364

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“…4 It is probably due to the petroleum distillates mixed with amitraz in commercial preparations 1 4 Convulsion Neurotoxic and proconvulsant effects are triggered by α 2 receptors partially 18 Polyuria α 2 adrenoceptor stimulation decreases antidiuretic hormone (ADH) and renin secretion, inhibition of ADH effect, and enhanced diuresis by increased glomerular filtration rate 43 Gastrointestinal hypomotility α 2 adrenoceptor stimulation causes hypomotility 46 47 Hyperglycaemia α 2 adrenoceptor stimulation reduces insulin secretion and causes hyperglycaemia. 36 The animal study conducted by Abu-Basha and colleagues 48 showed that amitraz inhibited insulin and stimulated glucagon secretion from the perfused rat pancreas, and inhibited insulin secretion no history of cardiac disease who recovered completely in 24 hours. We did not observe any changes in ECG in our cases.…”

Section: Miosis and Mydriasismentioning

confidence: 99%

Amitraz poisoning, an emerging problem: epidemiology, clinical features, management, and preventive strategies

Yılmaz¹

2003

Archives of Disease in Childhood

117

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Background: Amitraz is a pharmaceutical, veterinary, and agricultural product which is used worldwide under numerous generic names as an acaricide and insecticide. Because of its widespread use amitraz poisoning has come emerged as a cause of childhood poisoning during the past decade, particularly more in certain countries such as Turkey. Aims and Methods: To report the clinical features, the management, and the preventive strategies of amitraz poisoning in nine children, and review the previously reported 137 cases in humans. Results: Five male and four female children aged 10 months to 8 years were admitted to our department. The estimated ingested dose ranged between 89.2 and 163 mg/kg and estimated time from ingestion to presentation was 30-120 minutes. The initial signs and symptoms were impaired consciousness, drowsiness, vomiting, disorientation, miosis, mydriasis, hypotension, bradycardia, tachypnoea, hypothermia, and generalised seizures. Hyperglycaemia, glycosuria, and minimal increase in transaminase levels were observed. None required mechanical ventilation. CNS depression resolved spontaneously within 4-28 hours in all. The length of hospital stay was two to three days; all had a good outcome. Conclusion: This review details preventive measures and management strategies of amitraz poisoning, including the importance of following patients closely in the intensive care unit, monitoring their respiratory, cardiovascular, and central nervous systems since they may occasionally experience serious cardiopulmonary side effects.

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“…Yohimbine, an α2-adrenoceptor antagonist, prevented the amitraz induced hyperglycemia [36], CNS depression [37, 38], gastrointestinal effects, bradycardia [33, 35], sedation, loss of reflexes, hypothermia, hypotension, bradypnea and mydriasis [39]. Atipamezole, a new α2 adrenergic antagonist also prevented the effects of amitraz with less side effects compared to yohimbine [39].…”

Section: Discussionmentioning

confidence: 99%

“…The nonselective alpha-adrenoceptor antagonist tolazoline prevented some effects [37]. α1-adrenoceptor antagonist prazosin did not reverse the effects of amitraz [36, 37]. The muscarinic receptor antagonist atropine and the opioid receptor antagonist naloxone did not prevent the effects of amitraz on CNS.…”

Section: Discussionmentioning

confidence: 99%

Amitraz poisoning: A case report of an unusual pesticide poisoning in Sri Lanka and literature review

Herath

Pahalagamage

Yogendranathan

et al. 2017

BMC Pharmacol Toxicol

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BackgroundAmitraz is a pesticide used worldwide on animals and in agriculture. It contains triazapentadiene, which is a centrally acting alpha-2 adrenergic agonist. Amitraz poisoning is fairly uncommon in humans and occurs via oral, dermal or inhalational routes. Only a limited number of case reports of human intoxication have been published and most of them are of accidental ingestion by children.Case presentationA twenty-year-old Sri Lankan female presented following self-ingestion of 20 ml of amitraz resulting in 37.8 mg/ kg of amitraz poisoning. She lost consciousness after 20 min of ingestion, developed bradycardia and hypotension, which needed intravenous fluid resuscitation and dobutamine. Gastric lavage was performed. Her bradycardia persisted for 36 h and she was drowsy for 48 h. She did not develop respiratory depression, convulsions or hypothermia and the urine output was normal. Arterial blood gas revealed mild respiratory alkalosis. She recovered fully within 48 h and was discharged on day 3.ConclusionThe clinical manifestations of amitraz (impaired consciousness, drowsiness, vomiting, disorientation, miosis, mydriasis, hypotension, bradycardia, respiratory depression, hypothermia, generalized seizures, hyperglycemia and glycosuria) can be explained by the agonist action of amitraz on α1 and α2 receptors. Management of amitraz poisoning is still considered to be supportive and symptomatic with monitoring of nervous system, cardiovascular and respiratory systems. Activated charcoal may still be considered for treatment and the place for gastric lavage is controversial. Atropine is effective for symptomatic bradycardia and inotropic support is needed for hypotension that does not respond to fluid resuscitation. Diazepam or Lorazepam is used for convulsions and some patients may require intubation and ICU care. Several α2 adrenergic antagonists like yohimbine have been tried on animals, which have successfully reversed the effects of amitraz. Since the majority of amitraz poisoning cases are due to accidental ingestion, manufactures, regulatory authorities and national poisons control centers have a significant role to play in minimizing its occurrence.

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Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin

Cited by 23 publications

References 14 publications

Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review

Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review

Amitraz poisoning, an emerging problem: epidemiology, clinical features, management, and preventive strategies

Amitraz poisoning: A case report of an unusual pesticide poisoning in Sri Lanka and literature review

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