Pesticides and Chronic Diseases
William J. Rea, Kalpana D. Patel in Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
The leaked document, which was written by the EPA's Office of Chemical Safety and Pollution Prevention, explains clearly that “clothianidin's major risk concern is nontarget insects (honeybees)” and that acute toxicity studies to honeybees show that clothianidin is highly toxic on both a contact and an oral basis.”
Cytotoxicity and genotoxicity of clothianidin in human lymphocytes with or without metabolic activation system
Published in Drug and Chemical Toxicology, 2019
Zülal Atlı Şekeroğlu, Vedat Şekeroğlu, Ebru Uçgun, Seval Kontaş Yedier, Birsen Aydın
Clothianidin (CHN) is a novel and broad-spectrum neonicotinoid insecticide with a thiazolyl ring that exhibits excellent biological efficacy against varieties of pests (Tomizawa and Casida 2003, Liu et al.2017). Pharmacokinetic studies indicate that CHN is rapidly distributed into the entire body within 2 h after oral administration, and its excretion and metabolism immediately start after absorption. It is rapidly and almost completely eliminated from all tissues and organs with no evidence of accumulation. Most of it is completely excreted into urine and feces within two days after administration (Yokota et al.2003, Uneme et al.2006). The metabolic reactions of CHN in rats are: demethylation, denitration, formation of urea by hydrolysis, and cleavage of the carbon–nitrogen bond between the thiazolylmethyl and nitroguanidine moieties. After the reactions, further metabolic reactions also occur via glutathione conjugation of the thiazolyl ring (Uneme et al. 2006). The in vivo metabolic pathways of CHN in the liver microsomes of rats have been described. The major metabolic reactions (Phase I metabolism) are oxidative demethylation by microsomal CYP-450 enzymes to form N-(2-chlorothiazol-5-ylmethyl)-N-nitroguanidine. CHN is metabolized mainly to N-methyl-N-nitroguanidine and 2-methylthiothiazole-5-carboxylic acid, nitroguanidine, thiazolylnitroguanidine, thiazolmethylguanidine in Phase II metabolism (Calderon-Segura et al.2015).
Sub-lethal effects of thiamethoxam on Apis mellifera Linnaeus
Published in Toxin Reviews, 2022
Amit Choudhary, Bharathi Mohindru, Ashok Kumar Karedla, Jaspal Singh, Pardeep K. Chhuneja
Studies to elucidate the effect of a toxicant on learning and memory in honey bees were only possible with the development of assays based on Proboscis Extension Reflex (PER) behavior shown by a trained bee (Kuwabara 1957). The same technique was employed by El Hassani et al. (2008) to know the acute sub-lethal effect of acetamiprid and thiamethoxam on the behavior of honey bees in which it was found that thiamethoxam at 0.1, 0.5, and 1.0 ng bee−1 did not affect the learning or memory process in honey bees. In contrary to this, Aliouane et al. (2009) reported that honey bees having contact exposure chronically for 11 days to thiamethoxam (0.1 ng bee−1 day−1) had decreased olfactory memory (tested after 24 h after learning) or had a significant effect on learning performance. On this basis, the No Observed Effect Level (NOEL) of 0.003 ng µL−1 was proposed. Learning and memory in A. mellifera adults developed from larvae exposed chronically to thiamethoxam (0.6 ng bee−1) also got impaired (Papach et al.2017). Workers proposed that it is the clothianidin (a metabolized product of thiamethoxam, having a toxicity profile similar to its parent compound) that is responsible for negative effects on the memory process in bees.
Related Knowledge Centers
- Acetylcholinesterase
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- Nicotinic Acetylcholine Receptor
- Organophosphate
- Pyrethroid
- Thiamethoxam
- Imidacloprid
- Acetylcholine
- Carbamate