Acute and sub-acute toxicity effects of lambda-cyhalothrin in chicks

Article Highlights

1-   Lambda-cyhalothrin has a moderate toxic effect in chicks.

2-   Lambda-cyhalothrin causes behavioral and histological toxic effects, especially with high dose and exposure period (sub-acute).

3-   We do not recommend using this insecticide and restricted application of lambda-cyhalothrin in homes and agriculture is suggested.

Acute and sub-acute toxicity effects of lambda-cyhalothrin in chicks

S.A. Alrawe and M.H. Alzubaidy

Department of Physiology, Biochemistry and Pharmacology, College of Veterinary Medicine, University of Mosul, Mosul, Iraq

alrawe90@gmail.com, 0000-0003-4005-7215

munahazim@uomosul.edu.iq, 0000-0003-0986-9899, Corresponding author

Abstract

A Lambda-cyhalothrin (LTC) is classified as a synthetic type II pyrethroids, available in the local market, used to eliminate insects, which is widely used for spraying homes. This study aims to reveal the acute and subacute toxic effects of LTC in chicks as a biological model. The acute (LD₅₀) by up and down method recorded through 24 hrs. The signs and toxicity scores were estimated, the sub-acute toxicity effects of LTC in the open-field activity and tonic immobility test, body-weight and histopathological effects were recorded. The oral LTC LD₅₀ in chicks was 228.5 mg/kg. Oral administration of LTC at doses 57.12, 114.25, and 171.36 mg/kg, which represented 25%, 50%, and 75% of LD₅₀ respectively, caused signs of toxicity such asdepression with wing dropping, feathered by closed eyelids, gasping, and recumbency. LTC causes a significant decrease in chick’s weight, locomotor activity in the open field activity represented by increase latency to move, and decrease the number of lines crossed. The liver and brain show histopathological changes such as congestion, focal infiltration of mononuclear cells, hemorrhage, coagulative necrosis, and vasogenic edema. In the brain, the lesion was represented by shrunken in purkinji, demyelination of axon and hyper atrophy of astrocyte, the lesion was more severe in both organs when exposed to a high concentration and for longer periods. Our results demonstrated that LCT has a moderate toxicity in chicks, and causes behavioral and histological toxic effects, especially with sub-acute toxicity. Therefore, we do not recommend using it, and restricted application in homes and agriculture.

 Keywords: Lambda-cyhalothrin, Chicks, Toxicity effects, LD₅₀

التأثیرات السمیة الحادة وتحت الحادة للمبدا سیهالوثرین فی أفراخ الدجاج

شهد احمد الراویو منى حازم الزبیدی

فرع الفسلجة والکیمیاء الحیاتیة والأدویة، کلیة الطب البیطری، جامعة الموصل، الموصل، العراق

الخلاصة

یعد اللمبدا سیهالوثرین من المبیدات البایثرویدیة النوع الثانی ویستخدم بکثرة فی رش المنازل للقضاء على الحشرات ولتوفره فی الأسواق المحلیة. لذا کان الهدف من الدراسة الکشف عن التأثیرات السمیة الحادة وتحت الحادة فی نموذج أفراخ الدجاج. سجلت الجرعة الممیتة الوسطیة للمبدا سیهالوثرین بطریقة الصعود والنزول خلال 24 ساعة. کما تم تسجیل علامات التسمم الحادة ومراتب التسمم.تم دراسة التأثیرات السمیة تحت الحادة من خلال دراسة النشاط الحرکی والسلوک العصبی داخل المیدان المفتوح واختبار الاستجابة لعدم الحرکة الشدی کما تم قیاس أوزان الأفراخ واخذ المقاطع النسیجیة للکبد والدماغ. کانت الجرعة الممیتة الوسطیة للمبداسیهالوثرین 228.5 ملغم /کغم عن طریق الفم. أدى إعطاء اللمبدا سیهالوثرین عن طریق الفم بجرع 57.12,114.25,171.36 ملغم /کغم والتی تمثل 25و 50 و75 % من الجرعة الممیتة الوسطیة إلى ظهور علامات التسمم وکانت کالاتی؛ إغماض العینین وخمول ونفش الریش وتدلی الأجنحة وصعوبة التنفس والتغوط والرقود على عظم القص. سبب اللمبداسیهالوثرین انخفاضا معنویا فی أوزان الأفراخ وقلة فی الحرکة داخل المیدان المفتوح المتمثلة بزیادة وقت بدء الحرکة وقلة فی عدد الخطوط المقطوعة. أظهرت المقاطع النسیجیة للکبد احتقان وارتشاح بؤری للخلایا الالتهابیة أحادیة النواة ونزف وتنخر تجبنی وخزب. وکانت الآفات فی الدماغ هی انکماش خلایا برکنجی وإزالة النخاعین للمحور العصبی وضخامة الخلایا النجمیة العصبیة وکانت الآفات أکثر شدة عند استخدام المبید بتراکیز عالیة ولفترة طویلة. نستنتج من دراستنا الحالیة إن اللمداسیهالوثرین متوسط السمیة فی أفراخ الدجاج ویمتلک تأثیرات سمیة عصبیة متمثلة بالتغیرات السلوکیة والنسیجیة خلال التعرض لمدة 28 یوم تحت الحادة. لذا ننصح بالحد من استخدامه فی المنازل والمزارع.

Introduction

Lambda-cyhalothrin (LTC) is amongst the intensively used. Synthetic type II pyrethroids. It is a member of the new generation pyrethroids family (1). LTC has been considered as the favorite insecticide since it is relatively safe in terms of toxicity. It has been used for a broad range of crops, such as cotton and a variety of vegetables, to prevent parasites of plants. Furthermore, LTC has also been implemented in indoor usage for many purposes such as controlling mosquitos and other insects (1,2). LTC is utilized to control ticks, cockroaches, flies, and other disease vectors. Therefore, it may contribute to environmental hazards through the presence in water of rivers and streams, leading to poisoning of aquatic organisms, animals, and human. In addition, human poisoning with pyrethroids by eating contaminated beef has been recorded (2-4). Despite of LTC is moderately toxic for mammals (5,6), In fish, aquatic invertebrates, and bees, high toxicity has been observed. Lambda-cyhalothrin might be lethal at low concentrations in chicks, species (7). The lipophilic nature is important for the toxicity of lambda- cyhalothrin (8). As a result, pyrethroids are easily absorbed through membranes of the gastrointestinal system and respiratory system due to the high fat solubility, which also makes them easier to be stored in body fats, kidneys, liver, peripheral and central nervous systems (9). The liver is the organ responsible for metabolizing lambda-cyhalothrin and most the chemical compounds that enter the body through cleaving hydrolytic ester and oxidative pathways via the cytochrome P450 (CYP450), which yield reactive oxygen species (ROS). The excess production of ROS causes oxidative stress and cellular damage (10). Lambda- cyhalothrin's acute toxic impact is neurotoxicity. It impairs the production and transmission of nerve impulses by interfering with sodium channels in neurons. This action interferes with the nerve function of insects, causing loss of muscle control, paralysis, and death (9,10). Nerve fibers are the targets of the pyrethroids. They can impair the function of proteins regulating Na⁺ channels (<0.6%), in addition, they presumably affect both chloride and calcium channels, thereby impairing the nerve functions. As a result, the insect shows different bursts -ranging from short to long- due to repetitive signals discharge and nerve depolarization (10). Because the Lambda-cyhalothrin is cheap and available in the markets of Mosul, it is widely used for spraying at homes therefore, our current study sought to investigate the acute and subacute toxic effects in chicks.

Material and methods

Animals

We used 112 mix-breed Ross 7-28 days old broiler chicks of both males and females. They given water and ration ad libitum and were kept in batches of 20 to 30 chicks at a temperature of 30°C to 34°C, with constant lighting.

Insecticides and chemicals

Commercial pyrethroids insecticidal concentrate solutions of the lambda- cyhalothrin 5% manufactured by JU. AgriSciences Pvt. Ltd. India. The dose was 5 ml/kg administered orally.

Acute LD₅₀ of lambda-cyhalothrin

We determined the acute oral median lethal dose (LD₅₀) of lambda-cyhalothrin in broiler chicks using the up and down method (11). The signs of toxicity were recorded for two hours and then the lethality 24-hour was recorded, using 8 chicks for this experiment.

Acute toxicity signs of lambda-cyhalothrin in chicks

 We used 32 chicks age 7-14 days, of body weight 128-203 g, divided into four groups 8/group randomly. The dosages of lambda-cyhalothrin 0 control group, 57.12, 114.25, 171.36 mg/kg orally represented 25, 50, 75% of LD₅₀. The signs of poisoning were recorded within two hours. The severity of toxicosis was scored as reported earlier (12). The onset, signs, and toxicity score of lambda-cyhalothrin acute toxicity was evaluated for all groups.

Effect of lambda-cyhalothrin on open-field activity and tonic immobility

Twenty- four chicks were divided into four groups (6/group) randomly. The chicks were administered distilled water at 5 mL/ kg or lambda-cyhalothrin at 11.42, 22.85, 45.7 mg/kg orally these represented 5, 10 and 20% of LD₅₀. from the first day to the twenty-eighth day, measurements were taken on the seventh, fourteenth, and twenty- eighth days. The chicks were checked for behavior during 3 minute via open-field activity as mentioned earlier (13-16). Each chick was used for the tonic immobility behavioral paradigm, after the open-field activity test (13-16).

Effects of lambda-cyhalothrin on body weight of chicks:

Twenty- four chicks were weighed from the first day of dosing of lamda-cyhalothrin to the twenty-eighth day, and the average weights were taken on the seventh, fourteenth and twenty - eighth day.

Histological effects of lambda-cyhalothrin in the chicks.

The treated chicks with lambda-cyhalothrin at 0, 5, 10 and 20% of LD₅₀ mg/kg orally on the seventh, fourteenth, and twenty- eighth day were an incision was made, and 1 cm of liver and brain were obtained. Tissues were fixed using 10% neutral buffer formalin for 72 hours. Fixed tissues were processed according to the standard histopathological protocol, and thick slices 5-6 µm were stained using hematoxylin and eosin (17). Sections were examined under a light microscope, and images were taken using digital camera (HDCM-5).

Statistical analysis

Data were analyzed using one-way ANOVA, and then the significance was worked out via the least significant test. The Fisher test was used to analyze the frequency data. Non- parametric data were analyzed via Man Whitney test, using significance level at P

Results

Acute LD₅₀ of lambda-cyhalothrin in chicks

The acute LD₅₀ of lambda-cyhalothrin was 228.5 mg/kg orally by up and down technique (Table 1). The signs of poisoning are closed eyelids, depression with wing dropping, feathered, gasping, and immobility, recumbency, followed by death (Table 1).

Acute toxicity signs of lambda-cyhalothrin in chicks

Toxicity scores and acute toxicity signs of lambda-cyhalothrin are shown in table 2. Further, lambda-cyhalothrin at 57.12, 114.25 and 171.36 mg/kg orally that represented 25, 50 and 75% of acute LD₅₀, cause signs of poising in the chicks represented by closed eyelids, depression with wing dropping, feathered, defecation, twisting of the head, gasping, and recumbency.

Sub-acute effects of lambda-cyhalothrin on body weight of chicks

 Lambda -cyhalothrin at dose 11.42, 22.85, 45.7 mg/kg orally that represented 5, 10 and 20% of the acute LD_50, cause significant decrease in the body weight of the chicks on the seventh, fourteen and twenty-eight days compared to the control group (Tables 3-5).

Sub-acute effects of Lambda-cyhalothrin on the open-field activity and tonic immobility test.

Table 6 shows the effects of lambda-cyhalothrin on chicks treated with 11.42, 22.85 and 45.7 mg/kg orally, on the 7^th day of treatment, represented by significant drop in the number of line crossed, number of jumping and number of defecation compare with control group. The dose of lambda-cyhalothrin 45.7 mg/kg causes significant increase in the period to move in the arena compared to the control. Table 7 shows the effects of lambda-cyhalothrin in chicks treated with 11.42, 22.85 and 45.7 mg/kg orally on the 14^th day of treatment represented by a significant decrease in the number of line crossed, number of jumping and number of defecation in comparison with the control group and increase in the period to move in the arena compared to control group. Table 8 shown the effects of lambda-cyhalothrin in chicks treated with 11.42, 22.85, and 45.7 mg/kg orally on the 28^th day of treatment represented by a significant decrease in the number of line crossed compared to the control group at the dose 11.42 mg/kg and the dose of 45.7 mg/kg caused increase in the period to move in the arena compared to control group. Tables 6-8 shows the effects of lambda-cyhalothrin on chicks treated with 11.42, 22.85, and 45.7 mg/kg orally, the dose 45.7 causes a significant elevation in the period of tonic immobility test regarding to the control on the 7^th, 14th and 28^th days of treatment. On the 28^th day, all doses cause an increase in the period of immobility test.

Sub-acute effects of Lambda-cyhalothrin on the histopathological in the liver and brain

Figure 1 shows the microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-7 days of age show congestion and focal infiltration of mononuclear cells. We show in figure 2 the microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 22.85 mg /kg orally from 1-7 days of age fatty changes, with infiltration of inflammatory cells and hemorrhage. Whereas figure 3 shows the microscopic examination of liver in chicks treated with 45.7 mg/kg of lambda-cyhalothrin from 1-7 days of age coagulation necrosis, infiltration of inflammatory cells and hemorrhage. Figure 4 microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-14 days of age recent thrombus, vasogenic edema and vasculitis. In figure 5 microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 45.7 mg/kg orally from 1-14 days of age show recent thrombus, edema, and thickness of the wall of a portal artery and coagulative necrosis. The lesion is more severe in the liver treated with lambda-cyhalothrin at doses 11.41, 22.85 and 45.7 mg/kg orally from the age of 1-28 days, with the occurrence of the lesion shown in figure 6 when treating chicks at dose 22.85 mg/kg represented by hyperplasia of epithelial of the bile duct, edema, and dilation of the sinusoid.

In the brain treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-7 days of age show shrunken in Purkinje cells, congestion and vasogenic edema (Figures 7,8). In the pia meter section, we show a liquefactive necrosis, infiltration of inflammatory cells, congestion and necrotizing of blood vessels in the chicks treaded at dose 45.7 mg/kg, so the lesion was more sever in the dose 22.85 mg/kg (Figures 9,10). In figure 11, the microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 11.42 mg /kg orally from 1-14 days of age hyper atrophy of astrocyte, proliferation of astrocyte, demyelination of axon, vasogenic edema and infiltration of inflammatory cells. When performing histological examination of the chick’s brain, treated with the doses 22.85 and 45,7 mg/kg from 1-14 days of age, there are patches hemorrhage, sever infiltration of inflammatory cells, edema and liquefactive necrosis, more sever with dose 45.7mg/kg in figure 12. We show in figure 13 vascular degeneration in astrocyte, lysis of neuronal cell body and liquefactive necrosis in chicks treated with dose 11.42 mg/kg from 1-28 days of age. Whereas the chicks exposed to higher concentration of the lambda-cyhalothrin showed the histological lesions proven when performing a microscopic examination of the brain of the treated chicks for 28 days; profliration of oligodendroglia cells with longitudinal arrangement, hyper atrophy of astrocytes, demyelination of neuron axon, vasogenic edema and liquefactive necrosis (Figure 14).

Table 1: The acute LD₅₀ of lambda-cyhalothrin in chicks for 24 hour

*X: died; O: survived

 Table 2: Toxicity signs and toxicity scores of lambda-cyhalothrin in chicks

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P

Table 3: Bodyweight of chicks treated with lambda-cyhalothrin at dose 5, 10 and 20% of LD₅₀ at 7 days

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P

Table 4: Bodyweight of chicks treated with lambda-cyhalothrin at dose 5%, 10%and 20% of LD₅₀ at 14 days

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P

Table 5: Bodyweight of chicks treated with lambda-cyhalothrin at dose 5%, 10%and 20% of LD₅₀ at 28 days

Value means ± standard error. * Significantly dissimilar from the first group (control group) at P50) at P50) at P

Table 6: Effects of lambda-cyhalothrin in 3-minutes open field activity and tonic immobility test in the 7^th day from administration

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P50) at P50) at P

Table 7: Effects of lambda-cyhalothrin in 3-minutes open field activity and tonic immobility test in the 14^th day from administration

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P50) at P50) at P

Table 8: Effects of lambda-cyhalothrin in 3-minutes open field activity and tonic immobility test in the 28^th day from administration

Value means ± standard error. *Significantly dissimilar from the first group (control group) at P50) at P50) at P

Figure 1: Microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-7 days of age show a: congestion b: focal infiltration of mononuclear cells. HE, 40×1.1X.

Figure 2: Microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 22.85 mg /kg orally from 1-7 days of age show a: fatty changes b: with infiltration of inflammatory cells c: hemorrhage. HE, 40×2.2X.

Figure 3: Microscopic examination of liver in chicks treated with 45.7 mg/kg of lambda-cyhalothrin from 1-7 days of age show a: coagulation necrosis, b: infiltration of inflammatory cells, c: hemorrhage. HE, 40 × 1.6 X.

Figure 4: Microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-14 days of age show a: recent thrombus, b: vasogenic edema c: vasculitis. HE, 40× 1.2 X.

Figure 5: Microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-14 days of age show a: recent thrombus, b: vasogenic edema and c: vasculitis. HE, 40× 1.2 X.

Figure 6: Microscopic examination of liver in chicks treated with lambda-cyhalothrin at dose 22.85 mg/kg orally from 1-28 days of age show a: hyperplasia of epithelial of bile duct b: edema c: dilation of sinusoid. HE, 40×1.7X.

Figure 7: Microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-7 days of age show a: shrunken in Purkinje cells b: congestion. HE, 40 × 1.1 X.

Figure 8: Microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-7 days of age show a: shrunken of neuronal cell body b: vasogenic edema c: demyelination of axon. HE, 40×1.1X.

Figure 9: Microscopic examination of brain in chicks treated with 45.7 mg/kg of lambda-cyhalothrin from 1-7 days of age show a: liquefactive necrosis b: infiltration of inflammatory cells c: congestion d: necrotizing of blood vessels wall. HE, 40 ×1.4X.

Figure 10: Microscopic examination of brain in chicks treated with 45.7 mg/kg of lambda-cyhalothrin from 1-7 days of age show a: sever vascular degeneration. HE, 40×2.2X

Figure 11: Microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 11.42 mg /kg orally from 1-14 days of age show a: hyper atrophy of astrocyte b: proliferation of astrocyte c: demylination of axon d: vasogenic edema e: infiltration of inflammatory cells HE,40×1.3X

Figure 12: Microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 22.85 mg /kg orally from 1-14 days of age show a: patches hemorrhage b: sever infiltration of inflammatory cells c: edema d: liquefactive necrosis HE, 40×2.6X

Figure 13: Microscopic examination of brain in chicks treated with lambda-cyhalothrin at dose 11.42 mg/kg orally from 1-28 days of age show a: vascular degeneration in astrocyte b: lysis of neuron cell body c: liquefactive necrosis. HE, 40 ×1.5X.

Figure 14: Microscopic examination of brain in chicks treated with 45.7 mg/kg of lambda-cyhalothrin from 1-28 days of age show a: proliferation of oligodendroglia cells with longitudinal arrangement b: hypertrophy of astrocyte c: demyelination of neuron axon d: vasogenic edema e: liquefactive necrosis. HE, 40×1.2X.

Discussion

Due to the broad- spectrum, availability, and low price of lambda-cyhalothrin, and the limited information on the toxicity in avian, the effects of our current study spotlight on the acute and subacute toxicity of lambda-cyhalothrin in the chicks model. The LD₅₀ of lambda-cyhalothrin was 228.5 mg/kg orally in chicks, while the LD₅₀ in female rats was 56 mg/kg orally and 79 mg/kg orally in male rats (19). In mice, the LD₅₀ was 19.9 mg/kg orally (19), 416.22 mg/kg orally (20) in rabbit so that lambda-cyhalothrin is highly toxic in mice and rats and moderately toxic in chicks (19). The signs of acute toxicity estimated in this study such as depression and feathered, closed eyelids, wing drooping, defecation, twisting of the head, gasping and recumbency. While the clinical signs of acute oral neurotoxicity in the rat are ataxia, piloerection, salivation, lacrimation, as well as reducedmotor activity (21). Neurotoxicity is the primary acute toxic effect of lambda-cyhalothrin is; it can impair the function of proteins regulating Na⁺ channels. This results in a change in nerve function (10).

Sub-acute doses of lambda-cyhalothrin cause a significant decrease in the weight of chicks compared to the control group in the seventh, fourteenth and twenty-eight days. This result agrees with the study of (22,23). This may be attributed to the toxic effect, which reduces the intake and absorption of nutrients by the gut, and changed efficiency of food conversion rate, according to Ball and Chhabra (24). These results are in consistance with the findings of Yousef (23,25), who observed that treatment with lambda cyhalothrin reduces food consumption and weight gain in male rabbits. Different pyrethroids have been found to alter body weight as a result of exposure to this group of pesticides (26).

Our results revealed, the behavioral and histological changes observed in the liver and brain of chicks represented biomarkers for assessing insecticides toxicity. The values of this study in chicks treated with lambda-cyhalothrin at low toxic doses are decreased in open-field activity and increased in the tonic immobility test, especially at the dose 20 mg/kg. These behavioral changes are identical in cases of pyrethroids poisoning in subacute and chronic exposure (26,27) are agreement with the Mustafa and Al-Baggou in mice (28) and, Arulraj et al., (29). In fish tilapia, whereas increase activity and rapid swimming were reported by (29). The direct effect of the pesticide with interference of oxygen uptake and reducing brain cell respiration may be reason for damages seen in the brain (30). Furthermore, studies have proven the (CNS) central nervous system is the target organ of pyrethroids. Due to its high oxygen uptake, high pool of polyunsaturated fatty acids, and low levels of anti-oxidant mechanisms (31).

The most critical systemic effect of lambda-cyhalothrin was decreased motor activity. Pyrethroids insecticides are lipophilic in composition, which is absorbed via the (GIT), but also may incorporate into lipid-rich internal tissues, including body fat and the skin, liver, kidneys, ovaries, and nervous systems (32). The present results indicate that lambda-cyhalothrin causes hepatotoxicity with sub-acute toxicity. The histological sections of the liver treated with lambda-cyhalothrin insecticide show congestion, fatty changes, infiltration of inflammatory cells, coagulative necrosis, vasogenic edema and hyperplasia of epithelial sinusoid these results agree with the previous study in a rat of Fetoui et al. (32,33) in mice and Basir et al. (34) reported similar effects of the liver treated with lambda-cyhalothrin in rabbit and in fish. They suggested that oxygen free radicals and oxidative damage impact the pathogenesis of liver damage by elevating lipid peroxidation and reducing the activity of antioxidants (35). In addition, lambda-cyhalothrin induced hepatotoxicity in freshwater tilapia through its membrane destabilizing properties and peroxidation activities (36). Other pyrethroids, such as alpha-cypermethrin, induced the parenchymatous degeneration of hepatocytes in Swiss mice (26).

 Sections of the brain treated with LCT show shrunken in purkinji cells, congestion, vasogenic edema, demyelination of axon, liquefactive necrosis and infiltration of inflammatory cells and hypertrophy of astrocytes. Similar histopathological changes observed in the brain of mice treated with lambda-cyhalothrin by (36) and in rats (37). They reported tissue damage in the brain and liver, which might be due to the effect of reactive oxygen species (ROS) generated during insecticide metabolism (36, 37).

Conclusion

Lambda-cyhalothrin has a moderate toxic effect in chicks, and causes behavioral and histological toxic effects, especially with high dose and exposure period (sub-acute). Therefore, we do not recommend using this insecticide and restricted application of lambda-cyhalothrin in homes and agriculture is suggested.

Acknowledgement

Our study was supported by the College of Veterinary Medicine, University of Mosul, and Mosul, Iraq.

Conflict of interest

The authors financial claim does not have any interest.