Disposition and acute toxicity of imidacloprid in female rats after single exposure

Kapoor, Upasana; Srivastava, M. K.; Trivedi, Purushottam; Garg, Veena; Srivastava, L.P.

doi:10.1016/j.fct.2014.03.019

Cited by 72 publications

(44 citation statements)

References 26 publications

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“…One oral dose of imidacloprid equal to 20 mg kgG 1 b.wt. induced elevation of ALT and AST in blood of female rats (Kapoor et al, 2014). Monitoring imidacloprid and its metabolites (6-chloro nicotinic acid and 6-hydroxy nicotinic acid) were analyzed in brain, liver, kidney and ovary organs and blood and urine showed that the maximum concentration of imidacloprid and metabolites in each organ and bodily fluid occurred after 12 h (Kapoor et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Mammalian Detrimental Effects of Imidacloprid Residues in Tomato Fruits

Nassar¹,

Abbassy²,

Salem³

2015

Research J. of Environmental Toxicology

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Imidacloprid, a neonicotinoid pesticide, was used extensively to control whitefly (Bemisia tabaci) on tomato crop worldwide. Current study aimed to determine residue amounts of imidacloprid in tomato fruits after different time intervals of application and to evaluate their detrimental effects on white albino rats. Results revealed that the initial deposit (residue amount after 1 h of last spray application) was 0.316 mg kgG . Current study highlighted that there was no residual toxicity of imidacloprid after 14 days of last application.

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Section: Discussionmentioning

confidence: 99%

Mammalian Detrimental Effects of Imidacloprid Residues in Tomato Fruits

Nassar¹,

Abbassy²,

Salem³

2015

Research J. of Environmental Toxicology

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“…Imidacloprid residues in blood, liver, kidney, spleen, brain, lung, muscles and urine were determined. Three samples from each organ were extracted and cleaned up using QuEChERS modified method according to Lehotay (2007) and Kapoor et al (2014). The residues of IMI were determined using HPLC system (Agilent, USA) model 1100 series with the following conditions: a binary pump and auto sampler, UV (Ultra violet detector), BDS C 18 Equisil column (4.6 mm (id)×150mm length) and the mobile phase was distilled water and acetonitrile (30:70, V/V).…”

Section: Residue Analysesmentioning

confidence: 99%

“…Tissue disposition can provide important information on the time-course of compound transfer from one tissue compartment to another. Kapoor et al (2014) used QuEChERS, which stands for quick, easy, cheap, effective, rugged, and safe method for analysis the residues of IMI in different organs (liver, brain, kidney and ovary) and body fluids (blood, urine and faeces).…”

Section: Introductionmentioning

confidence: 99%

Enzyme Activity and Time-Course Quantitative Distribution of an Oral Dose of Imidacloprid in Male Rat Tissues

Nasr

Shalaby

Ragheb

et al. 2019

Zagazig Journal of Agricultural Research

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The purpose of this study was to investigate the time course of changes in enzymes activity during distribution of imidaclopride (IMI) in Male Albino rat (Rattus norvegicus) after 1, 3, 6, 12, 24 and 48 hr., treatment with a single oral dose (20 mg/kg body weight). The results showed significant gradual increase in liver and kidney function parameters coincided with accumulation of imidacloprid with varying quantities according to each organ, then gradually decreased to the end of study. The highest activity in liver enzymes, ALT (97.33 U/L), AST (78 U/L) ALP (169.66 IU/L) and LDH (5190.67 U/L) was recorded six hours post treatment, as well as increasing in total protein (8.94 g/dl). Kidney function parameters, i.e. urea, creatinine and uric acid levels (75.67, 2.283, 19.15 mg/dl, respectively) were also revealed the highest increase comparing with control. Liver and brain acetylcholinesterase (AChE) activity was reached the lowest level with the inhibition percent 82.9, 81.4%, respectively at the same time agreed with the concentration peak of IMI in blood (8.04 µg/ml) liver (2.42 µg/g) and brain (4.06 µg/g). The trend of maximal concentration of IMI in different organs and body fluids at six hours post dosing was in the following order: urine > blood > lungs > brain > testes > spleen > kidney > liver > muscles.

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“…Hepatic impairment occurred mostly due to exposure to toxic chemicals, environmental pollutants for the last few decades (Atta et al, 2010). The hepatotoxicity of neonicotinoids is measured by evaluating the enzymatic activity and liver histopathological changes, which were degeneration of hepatocytes, central vein dilations, and elevation of liver enzymes (Toor et al, 2013;Vohra et al, 2014;Kapoor et al, 2014). Ginger, the rhizome of Zingiber officinale Roscoe (a member belonging to the Zingiberaceae family) are commonly used as a spice or dietary supplement with a long history of utilization in the traditional medicine (Yusof, 2016).…”

Section: Introductionmentioning

confidence: 99%

Modulatory Effect of Ginger Aqueous Extract on Imidacloprid Induced Hepatotoxicity in Rats

Farag¹,

Fotoh²,

EL-Sayed³

et al. 2019

Adv. Anim. Vet. Sci.

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The current study was conducted for evaluation of the hepatotoxic effect of Imidacloprid (IMI) in rats and to assess the modulatory role of Zingiber officinale Roscoe, ginger aqueous extract (GAE), against such effect. Sixty mature male rats (Rattus norvegicus) were utilized and divided into six groups (10 each); group 1 was negative control received 0.1 ml of distilled water, group 2 was positive control which received 1ml of GAE, group 3 administered with 0.1 ml of IMI, group 4:administered 1ml of GAE for 2 weeks followed by administration of 0.1ml of IMI (served as protected group), group 5 administered with 0.1 ml of IMI then 1ml of GAE for 2 weeks (served as treated group) and the last group simultaneously administered with 0.1ml of IMI and 1ml of GAE (served as combination group). Oral dosing of IMI and GAE was triple weekly (day after day) and the experimental period was three months for all groups. IMI exposure caused significant increase in alanine aminotransferase (ALT), aspartate amino transferase (AST) levels, significant decrease in total proteins, albumin and globulins in serum, IMI upregulates interleukin 6 (IL 6), tumor necrosis factorα (TNF-α) and toll like receptor 2 (TLR2) genes in the liver of rats associated with intense immuno positive reactivity of TLR2 and TNF α in the liver of IMI-treated group. Histopathological examination revealed significant alterations in the liver tissue of IMI-treated group, such as disorganization of hepatic cords replaced by mononuclear cells which surrounded by lymphocytes and mild congestion of blood vessels was also seen. In conclusion, the IMI hepatotoxic effect could be modulated by the use of GAE.

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Disposition and acute toxicity of imidacloprid in female rats after single exposure

Cited by 72 publications

References 26 publications

Mammalian Detrimental Effects of Imidacloprid Residues in Tomato Fruits

Mammalian Detrimental Effects of Imidacloprid Residues in Tomato Fruits

Enzyme Activity and Time-Course Quantitative Distribution of an Oral Dose of Imidacloprid in Male Rat Tissues

Modulatory Effect of Ginger Aqueous Extract on Imidacloprid Induced Hepatotoxicity in Rats

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