C H A P T E R
49
Amitraz
Ramesh C. Gupta
INTRODUCTION
Amitraz is a triazapentadiene compound, which is a
member of the formamidine pesticide family. It has a
chemical formula of C19H23N3 and molecular weight
293.41. Its chemical structure is shown in Figure 49.1.
Amitraz is commonly used in agriculture and horticul-
ture as an insecticide and acaricide to control red spider
mites, leaf miners, scale insects, aphids and other infes-
tations. Amitraz is currently approved in the United
States for various applications, including use on both
food producing and companion animals. It is used to
control ticks, mites, lice and many other pests on dogs,
sheep, cattle and pigs. Amitraz is available as a wetable
or pour-on powder, an emulsifiable liquid and a spray. It
is also used as an active ingredient in formulations with
other insecticides, such as metaflumizone (ProMeris®).
Amitraz is sold under various product names, including
Aazdieno, Acadrex, Acarac, Adrizan, Aludex, Amitik,
Amitraze, Avartin, Baam, Bumetran, Ectodex, Edrizan,
Kenaz, Mitac, Maitac, Metaban, Mitaban, Preventic,
Ridd, Tickoff, Taktic, Triatix, Ovasyn, Ovidrex and many
others. Of course, Mitaban, Preventic and Taktic are the
three most popular brand names for amitraz. Amitraz
poisoning is frequently encountered in dogs and cats
(Grossman et al., 1993; Gunaratnam et al., 1993; Hugnet
et al., 1996; Andrade et al., 2004). In humans, poison-
ing occurs due to widespread use of amitraz veterinary
products (Ertekin et al., 2002; Proudfoot, 2003; Yilmaz
and Yildizdas, 2003; Aagin et al., 2004; Avsarogullari
et al., 2006). Amitraz is not recommended for use in cats
and horses as it causes toxicity. This chapter describes
the toxicity of amitraz in animals with a special focus on
dogs and cats.
Veterinary Toxicology, Edited by Ramesh C. Gupta
ISBN: 978-0-12-385926-6
599
BACKGROUND
Amitraz is a broad spectrum insecticide and acaricide
used in veterinary medicine and in agriculture and
horticulture throughout the world since 1974. Amitraz
has rapid action on the control of animal ectoparasites,
such as mites, ticks, lice, etc., and it persists on hair and
wool long enough to control all stages of the parasite.
Amitraz was a restricted use pesticide in 1985 because
some studies showed it caused cancer in mice. But re-
evaluation of the evidence has led to the current clas-
sification of amitraz as an unrestricted or general use
pesticide. In veterinary medicine, the most common
use of amitraz is in tick collars, which contain 9% ami-
traz as an active ingredient. A collar for a large size dog
contains 2.4 g of amitraz (Hugnet et al., 1996). Amitraz
is available as a 19.9% topical solution for dogs. All tic-
kicide dips for cattle and sheep contain 0.025% amitraz
as the active ingredient. In France, tick collars contain
8–9% amitraz, and external lotions contain 5–12.5% ami-
traz. The amitraz-containing product Metaban, which
is a liquid concentrate and labeled for veterinary use, is
commonly used for demodectic mange (Demodex canis)
in dogs (Farmer and Seawright, 1980). Amitraz is also
used to control ectoparasites on cattle, sheep, goats and
pigs. Amitraz is not recommended for cats and horses
(Auer et al., 1984; Gunaratnam et al., 1993). There are
several reports that have described amitraz poisoning
in animals (Roberts and Argenzio, 1979; Turnbull, 1983;
Auer et al., 1984; Hsu et al., 1984; Grossman et al., 1993;
Hugnet et al., 1996; Andrade et al., 2004). With dogs, poi-
soning is most often associated with accidental ingestion
of the collar, resulting in severe toxicity and sometimes
fatal poisoning (Grossman et al., 1993; Hugnet et al.,
© 2012 Elsevier Inc. All rights reserved.
DOI: 10.1016/B978-0-12-385926-6.00049-1
600 49. AMITRAZ
H3C CH3 H3C CH3
N N N
CH3
FIGURE 49.1 Chemical structure of amitraz.
1996). Amitraz should not be used in diabetic animals as
it adversely affects the levels of glucose and insulin (Hsu
and Schaffer, 1988).
PHARMACOKINETICS/
TOXICOKINETICS
Amitraz is a highly lipid soluble compound that is rap-
idly absorbed following oral ingestion or dermal appli-
cation, thus making exposure potentially dangerous
for animals as well as humans. In the stomach, amitraz
can be metabolized to as many as six metabolites and
some of them are potentially toxic. Dogs receiving ami-
traz (100 mg/kg, PO) in a gelatin capsule revealed the
pharmacokinetic parameters as follows: area under the
curve (AUC0-48 h 5 265.3 6 12.3 mg/h/ml), elimination
t½ (23.4 6 2.3 h), time to reach peak plasma concentration
(tmax 5 5.0 6 0.7 h), and mean peak plasma concentra-
tion (Cmax 5 20.7 6 2.3 mg/L) (Hugnet et al., 1996). From
these data it is clear that amitraz has a long elimination
half-life and a significant amount is absorbed, which is
accountable for most of the observed signs. There is a
strong association between plasma amitraz concentra-
tions and clinical manifestations in dogs (Hugnet et al.,
1996). Recently, Marafon et al. (2010) reported similar
findings in cats experimentally intoxicated with 0.4%
amitraz bath dip, which was eight times greater than
the recommended concentration. Hugnet et al. (1996)
observed that clinical signs of toxicosis usually appeared
around 1 h after ingestion, with plasma concentration
around 5 mg/L, and signs lasted until the concentra-
tion of amitraz decreased. This information can be used
to monitor accidental ingestion of amitraz by dogs. In
ponies and sheep, amitraz has a brief half-life after intra-
venous (IV) administration because it is hydrolyzed in
the blood by formaminidases (Pass and Mogg, 1995).
The two major metabolites of amitraz are 2,4-dime-
thyl-formanilide and N-(2,4-dimethylphenyl)-N9-
methylformamidine. The former metabolite is a
relatively weak methemoglobin-former in dogs and
man. These metabolites are further catabolized to
2,4-dimethylaniline and ultimately to 4-amino-3-meth-
ylbenzoic acid, which is the principal metabolite found
in the urine and liver (Aronson et al., 1988; Jones, 1990).
In essence, amitraz and its metabolites are excreted
primarily in the urine and feces.
MECHANISM OF ACTION
Amitraz kills mites, ticks and other parasites by interfer-
ing with their nervous system. The tick’s sharp barbed
mouth parts become paralyzed and cannot pierce the
skin, thereby inhibiting the tick from feeding on dogs.
Attached ticks will then detach.
Amitraz in higher doses has been shown to produce
toxicity in several animal species by stimulating α2-
adrenergic receptors (α2-AR) resulting in impairment
of consciousness, respiratory depression, convulsions,
bradycardia, hypotension, hypothermia and hypergly-
cemia. In early studies, amitraz produced effects simi-
lar to that produced by a pure α2-AR agonist drug such
as clonidine (Costa et al., 1988; Jorens et al., 1997). In a
recent experimental study, Marafon et al. (2010) observed
significant declines in heart rate and respiration rate
of cats intoxicated with amitraz. Electrocardiography
(ECG) on an amitraz-poisoned English bulldog revealed
prolonged QT intervals (Malmasi and Ghaffari, 2010).
Amitraz acts centrally to influence blood pressure and
heart rate by α2-AR agonism which causes a reduction in
peripheral sympathetic tone (Kobinger, 1978; Cullen and
Reynoldson, 1990). In the peripheral vasculature, both
α1 and α2-ARs are involved in contributing to the vaso-
pressor action of amitraz which results in hypotension.
It is suggested that the central α2-AR agonist activity of
amitraz is responsible for CNS depression (Cullen and
Reynoldson, 1990).
In addition to being an α2-AR agonist, amitraz is a
potent inhibitor of the enzyme monoamine oxidase
(MAO), which is responsible for degrading the neuro-
transmitters norepinephrine and serotonin, resulting in
behavioral and neurotoxic effects (Aziz and Knowles,
1973; Moser and Macphail, 1988). Amitraz is also known
to cause inhibition of prostaglandins (Yim et al., 1978).
TOXICITY
Acute toxicity
Acute toxicity data of amitraz is available for laboratory
animals. Oral LD50 is 650 mg/kg in rats and 1600 mg/kg
in mice. Values of dermal LD50 in rabbits and rats are
.200 mg/kg and 1600 mg/kg, respectively. Oral LD50 val-
ues of amitraz for dog, pig, guinea pig and baboons are
reported to be 100, 100, 400 and 100 mg/kg, respectively.
The inhalation LC50 (6 h) of amitraz for rats is 65 mg/L
 TOXICITY
of air. The oral LD50 in birds (bobwhite) is estimated at
788 mg/kg, and dietary LD50 in mallard is 7000 mg/kg
and in Japanese quail is 1800 mg/kg. LC50 is 0.74 ppm
in rainbow trout, 0.5 ppm in bluegill and 3.2–4.2 ppm in
harlequin fish. The EPA classifies amitraz as a Class III
slightly toxic pesticide.
Signs of acute amitraz poisoning in male and female
rats treated with 440 mg/kg and 365 mg/kg, respec-
tively, include coolness to touch, reduced spontaneous
activity, increased episodes of activity, such as aggres-
sion in response to handling, and signs of debilitation
(Hayes and Laws, 1991). Due to its widespread use,
acute amitraz poisoning is often encountered in dogs
and cats. Poisoning may occur by oral, inhalation or der-
mal exposure, but poisoning is most often via the oral
route. Onset of clinical signs is noted within 30 min to
2 h after ingestion. Clinical signs of poisoning include
GI disturbance, nausea, vomiting, diarrhea, staggering,
disorientation, CNS and respiratory depression, brady-
cardia, hypotension and hypothermia. Biochemical
changes include hyperglycemia and elevation of liver
enzyme (transaminases) activity. In dogs, following a
topical application, amitraz has been shown to increase
plasma glucose and decrease insulin release when
dogs were dipped at twice the recommended concen-
tration (Hsu and Schaffer, 1988). When amitraz is for-
mulated in xylene and propylene oxide, signs such as
depression, ataxia, stupor and coma are likely attrib-
uted to the xylene and propylene oxide (Jones, 1990).
Generally, signs and symptoms of amitraz poisoning
subside within 24–48 h, while in some cases it may take
7–10 days.
In dogs and cats, common side effects of the pesti-
cide include anorexia, sedation and a dry skin and hair
coat. Serious side effects include low blood pressure,
hypothermia, hyperglycemia, mydriasis, bradycardia,
slow intestinal rate, incoordination, ataxia, vasoconstric-
tion, vomiting, diarrhea, seizures and in rare instances
death. Animals exposed to amitraz may show signs
of CNS stimulation or CNS depression, depending on
the dose level and to some extent the species involved.
Generally, at low doses CNS stimulation may occur, as
manifested by hyperactivity to external stimuli such as
handling and considerably increased food consumption
(Pfister and Yim, 1977). High doses of amitraz have a
CNS depressive effect with reduced spontaneous activ-
ity, bradycardia, respiratory depression and hypother-
mia. Oglesby et al. (2006) observed renal cortical necrosis
and hemorrhage in a dog, which died from acute renal
failure following ingestion of an amitraz-formulated dip.
Untreated dogs and cats usually go into a coma and die
from respiratory failure. Surviving animals show com-
plete recovery from all signs and symptoms in about
7–10 days, even when exposed to higher doses (Bonsall
and Turnbull, 1983).
601
Evidence from animal studies suggests that amitraz
is a neurotoxicant (Moser and Macphail, 1988). Amitraz
has been shown to produce many behavioral and physi-
ological changes in rats. Amitraz at a dose greater than
100 mg/kg caused inhibition of monoamine oxidase
(MOA) within 2 h of dosing and lasted up to 7 days.
Amitraz appears to be more selective for type B-MAO
when given in vivo, although MAO-A was also inhibited
at doses $300 mg/kg. However, no selectivity was indi-
cated by the IC50 values determined in vitro (IC50 5 31 and
28 µM for MAO-A and MAO-B, respectively). Findings
revealed that the MAO inhibition is probably not due to
amitraz-induced alterations in motor activity. Amitraz
produced only negligible inhibition of acetylcholineste-
rase at very high doses. In a dose-dependent manner,
amitraz produced depressed arousal and rearing activity,
hypothermia, body weight loss; and autonomic changes
including ptosis, mydriasis, chromodacryorrhea resulting
in facial crustiness, loss of the pupil reflex and decreased
defecation in rats (Moser, 1991).
Horses poisoned by amitraz may show clinical signs
of tranquilization, depression, ataxia, muscular incoor-
dination and impaction colic that can last up to a week,
followed by mild dehydration and acidosis.
Chronic toxicity
In chronic 2-year feeding trials, rats receiving 50 mg/kg/
day in their diet or dogs receiving 0.25 mg/kg/day of
amitraz did not show any ill effects. Dogs given
1 mg/kg/day exhibited signs of slight CNS depression
and hypothermia, and blood analysis revealed signifi-
cant hyperglycemia.
Studies suggest that amitraz exerts endocrine dis-
rupting activity and reproductive and developmen-
tal toxicity. Male and female rats receiving amitraz at
200 mg/kg/day for 10 weeks showed decreased fertil-
ity. Female mice treated with amitraz orally (50 mg/
kg/day) for 5 days and then mated showed a slight
increase in loss of fetuses and a decrease in the number
of living offspring. When male mice were given the same
dose for the same duration and then mated, the result-
ing embryos were significantly less likely to grow in the
mother’s uterus. Rabbits who received 25 mg/kg/day of
amitraz from days 6 to 18 of pregnancy had fewer and
smaller litters (Meister, 1994).
Being an α2-AR agonist, amitraz is reported to
adversely affect the mammalian reproductive system by
binding to presynaptic α2-AR in the hypothalamus, thus
inhibiting noradrenalin release and decreasing gonado-
tropin-releasing hormone secretion (Altobelli et al., 2001).
In addition, several in vivo and in vitro studies have
demonstrated that amitraz is a reproductive toxicant
(Goldman and Cooper, 1993; Young et al., 2005).
602 49. AMITRAZ
Amitraz also has the potential for teratogenic activity.
In rats treated with 12 mg/kg/day of amitraz from day
8 to 20 of pregnancy, the offspring were heavier but had
less bone development than the offspring of untreated
rats (Hayes and Laws, 1991). In a recent investigation,
Kim et al. (2007) showed that amitraz administered
during the entire pregnancy period in rats is embryo-
toxic and teratogenic at the maternally toxic dose (i.e.,
30 mg/kg/day) and is minimally embryotoxic at a mini-
mal maternally toxic dose (i.e., 10 mg/kg/day). Amitraz
and its metabolite 2,4-dimethylaniline have also been
shown to induce teratogenic effects in frog embryos
(Osano et al., 2002).
Studies in laboratory animals have shown that ami-
traz has no potential for mutagenic activity and does not
cause damage to DNA (Hayes and Laws, 1991). Amitraz
can cause tumors in female mice but not in male mice or
male or female rats. EPA has established the teratogenic
no observed effect level (NOEL) in rats at 12 mg/kg/day
(Walker and Keith, 1992). The teratogenic NOEL in rab-
bits is 25 mg/kg/day.
Diagnosis
Most of the time, poisoning in animals (especially dogs
and cats) with amitraz is acute. Diagnosis is based on
history of exposure, presence of the collar’s pieces in
the stomach on X-ray, clinical signs of toxicity associ-
ated with stimulation of α2-AR, and residue analysis.
Due to a long half-life, residue of amitraz and its major
metabolites can be detected in the plasma of a poisoned
animal using GC coupled with a nitrogen–phosphorus
detector or a thermionic-specific detector (Ameno et al.,
1991; Marafon et al., 2010), or HPTLC coupled with a UV
detector (Hugnet et al., 1996).
TREATMENT
In most cases, symptomatic and supportive therapies
are of great value. Remove the tick collar or any other
source of amitraz from pets. IV fluids are recommended.
In the case of dermal exposure, bathing is helpful. For
oral ingestion, induction of vomiting and gastric lavage
is recommended. Administration of activated charcoal
with a saline cathartic is also beneficial. Animals should
be kept in the warm, as amitraz causes hypothermia.
Continuous monitoring of cardiovascular, respiratory
and central nervous systems, and of glucose and insulin
levels is advised.
Studies from animals suggest that the α2-AR antago-
nists (yohimbine and atipamezole) can reverse amitraz-
induced toxicity. In dogs, yohimbine has been found to
be very effective. Bradycardia and hypotension respond
to yohimbine administration (Hsu and Schaffer, 1988).
Dogs severely poisoned with amitraz have been success-
fully treated with low doses (50 µg/kg, IM) of the potent
α2-AR antagonist atipamezole (Hugnet et al., 1996).
Doses of atipamezole can be repeated after 3 to 4 h, if
necessary. Atipamezole can control all the clinical effects
of amitraz within 20 min. With good care and aggressive
treatment, even severe cases can be recovered.
CONCLUSIONS
Amitraz is widely used as an insecticide and acaricide in
veterinary medicine. Dogs and cats are intoxicated due
to accidental ingestion of amitraz-containing tick collars
and other products. Major toxic signs are associated with
α2-adrenergic receptor (α2-AR) agonism, such as CNS
depression, hypotension, bradycardia, and hypothermia.
Increased blood glucose and decreased insulin secretion
are characteristics of amitraz poisoning and are also due
to α2-AR stimulation. With timely administration of an
α2-AR blocker (yohimbine or atipamezole), and conven-
tional therapeutic measures, even seriously intoxicated
cases can recover.
ACKNOWLEDGMENTS
I would like to thank Mrs. Robin B. Doss and Ms.
Michelle A. Lasher for their assistance in the preparation
of this chapter.
REFERENCES
Aăgin H, Calkavur Ö, Uzun H, Bak M (2004) Amitraz poisoning:
clinical findings. Indian Pediatr 41: 482–486.
Altobelli D, Martire M, Maurizi S, Preziosi P (2001) Interaction of
formamidine pesticides with the presynaptic alpha(2)-adreno-
ceptor regulating. Toxicol Appl Pharmacol 172: 179–185.
Ameno K, Fuke C, Ameno S, et al. (1991) A rapid and sensitive
quantitation of amitraz in plasma by gas chromatography with
nitrogen-phosphorus detection and its application for pharma-
cokinetics. J Anal Toxicol 15: 116–118.
Andrade SF, Salnchcz O, Tostes RA (2004) Relato de 5 casos de
intoxicacao por amitraz cm cacs c. gatos. Clin Veterinaria 53:
38–42.
Aronson CE, Powers TE, Davis LE (1988) Veterinary Pharmacological
Biology, 6th edn. Veterinary Medicine Publishing Co., Lenexa,
Kansas. pp. 905–906.
Auer DE, Seawright AA, Pollitt CC, Williams G (1984) Illness in
horses following spraying with amitraz. Aust Vet J 61: 257–259.
 REFERENCES
Avsarogullari L, Ikizceli I, Sungur M, Sözüer E, Akdur O, Yücei M
(2006) Acute amitraz poisoning in adults: clinical features, labo-
ratory findings, and management. Clin Toxicol 44: 19–23.
Aziz SA, Knowles CO (1973) Inhibition of monoamine oxidase by
the pesticide chlordimeform and related compounds. Nature
242: 417–418.
Bonsall JL, Turnbull GJ (1983) Extrapolation from safety data to
management of poisoning with reference to amitraz and xylene.
Human Toxicol 2: 587–592.
Costa LG, Olibet G, Murphy SD (1988) Alpha-2 adrenoceptors as a
target for formamidine pesticides. In vitro and in vivo studies in
mice. Toxicol Appl Pharmacol 93: 319–328.
Cullen LK, Reynoldson JA (1990) Central and peripheral alpha-
adrenoceptor actions of amitraz in the dog. J Vet Pharmacol Ther
13: 86–92.
Ertekin V, Alp H, Selimoglu M, Karacan M (2002) Amitraz poison-
ing in children: retrospective analysis of 21 cases. J Intl Med Res
30: 203–205.
Farmer H, Seawright AA (1980) The use of amitraz
(N9-2,4(dimethylphenyl)-N-[(2,4-dimethylphenyl) imino)-methyl]-
N-methylmethanimidamide) in demodecosis in dogs. Aust Vet J
56: 537–541.
Goldman JM, Cooper RL (1993) Assessment of toxicant-induced
alterations in the luteinizing hormone control of ovulation in the
rat. In Female Reproductive Toxicology, Chapin H (ed.), Academic
Press, San Diego, CA, pp. 79–91.
Grossman MR, Garvey MS, Murphy MJ (1993) Amitraz toxicosis
associated with ingestion of an acaricide collar in a dog. J Am
Vet Med Assoc 203: 55–57.
Gunaratnam P, Wilkinson GT, Seawright AA (1993) A study of ami-
traz toxicity in cats. Aust Vet J 60: 278–289.
Hayes WJ, Laws ER, Jr (1991) Handbook of Pesticide Toxicology, Vol. 1.
Academic Press, Inc., New York, NY.
Hsu WH, Lu ZX, Hembrough FB (1984) Effects of amitraz on heart
rate and aortic blood pressure in conscious dogs; influence
of atropine, prazosin, talazoline, and yohimbine. Toxicol Appl
Pharmacol 84: 418–422.
Hsu WH, Schaffer DO (1988) Effects of topical application of ami-
traz on plasma glucose and insulin concentrations in dogs. Am J
Vet Res 49: 130–131.
Hugnet C, Buronfusse F, Pineau X, Cadore J-L, Lorgue G, Berney PJ
(1996) Toxicity and kinetics of amitraz in dogs. Am J Vet Res 57:
1506–1510.
Jones RD (1990) Xylene/amitraz: a pharmacologic review and pro-
file. Vet Human Toxicol 32: 446–448.
Jorens PG, Zandijk E, Belmans L, Schepens PA, Bossaert LL (1997)
Hum Exp Toxicol 16: 600–601.
Kim JC, Shin JY, Yang YS, Shin DH, Moon CJ, Kim SH, Park SC,
Kim YB, Kim HC, Chung MK (2007) Evaluation of develop-
603
mental toxicity of amitraz in Sprague-Dawley rats. Arch Environ
Contam Toxicol 52: 137–144.
Kobinger W (1978) Central alpha-adrenergic system as targets for
hypersensitive drugs. Rev Phys Biochem Pharm 81: 39–100.
Malmasi A, Ghaffari S (2010) Electrocardiographic abnormalities in
an English bulldog with amitraz toxicity. Comp Clin Pathol 19:
103–105.
Marafon CM, Delfim CIG, Valadao CAA, Menotti R, Andrade SF
(2010) Analysis of amitraz in cats by gas chromatography. J Vet
Pharmacol Ther 33: 411–414.
Meister RT (1994) Farm Chemicals Handbook. Meister Publishing Co.,
Willoughby, OH.
Moser VC (1991) Investigations of amitraz neurotoxicity in rats. IV.
Assessment of toxicity syndrome using a functional observa-
tional battery. Toxicol Sci 17: 7–16.
Moser VC, Macphail RC (1988) Investigations of amitraz neurotox-
icity in rats. Effects on motor activity and inhibition of monoam-
ine oxidase. Toxicol Sci 12: 12–22.
Oglesby PA, Joubert KE, Meiring T (2006) Canine renal cortical
necrosis and hemorrhage following ingestion of an amitraz-for-
mulated insecticide dip. J S Afr Vet Assoc 77: 160–163.
Osano O, Oladimeji AA, Kraak MHS, Admiral W (2002) Teratogenic
effects of amitraz, 2,4-dimethylaniline, and paraquat on devel-
oping frog (Xenopus) embryos. Arch Environm Contam Toxicol 43:
22–49.
Pass MA, Mogg TD (1995) Pharmacokinetics and metabolism of
amitraz in ponies and sheep. J Vet Pharmacol Ther 18: 210–215.
Pfister W, Yim GKW (1977) Formamidine induced feeding and
behavioral alteration in the rat. Fed Proc 36: 352–353.
Proudfoot AT (2003) Poisoning with amitraz. Toxicol Rev 22: 71–74.
Roberts MC, Argenzio A (1979) Amitraz induced large intestinal
impaction in the horse. Aust Vet J 55: 553–554.
Turnbull GJ (1983) Animal studies on the treatment of poisoning
by amitraz (a formamidine pesticide) and xylene. Human Toxicol
2: 579–586.
Walker MM, Keith LH (1992) EPA Fact Sheet Database. Lewis
Publishers, Ann Arbor, MI.
Yilmaz HL, Yildizdas DR (2003) Amitraz poisoning, an emerging
problem: epidemiology, clinical features, management, and pre-
ventive strategies. Arch Dis Childhood 88: 130–134.
Yim GKW, Holsapple MP, Pfister WR, Hollingworth RM (1978)
Prostaglandin synthesis inhibited by formamidine pesticides.
Life Sci 23: 2509–2516.
Young FM, Menadue MF, Lavranos TC (2005) Effects of the insecti-
cide amitraz, an α2-adrenergic receptor agonist, on human lutei-
nized granulosa cells. Human Reprod 20: 3018–3025.