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Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
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.”
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
Among various neonicotinoids, midacloprid was the first commercial product launched by the Nihon Tokushu Nohyaku (now Nihon Bayer) in 1991 which was followed by thiamethoxam (a Syngenta product) in the year 1992. These compounds have remarkable insecticidal properties against sucking insect pests, hence quickly dominating the world market by acquiring a share of 25 and 80% in general and seed treatment application, respectively (Jeschke et al.2011). Thiamethoxam is also a precursor of clothianidin (an open-chain neonicotinoid) both in plants and insects (Nauen et al.2003). As per Iwasa et al. (2004) both have comparable toxicity to bees (LD50 of clothianidin and thiamethoxam as 22 and 30 ng, respectively). The residues of clothianidin accumulated in bees only after chronically feeding the bees with thiamethoxam (Coulon et al.2019).
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).
Crocin-protected malathion-induced spatial memory deficits by inhibiting TAU protein hyperphosphorylation and antiapoptotic effects
Published in Nutritional Neuroscience, 2020
Leila Mohammadzadeh, Khalil Abnous, Bibi Marjan Razavi, Hossein Hosseinzadeh
The MWM is widely used for the study of spatial learning and memory. Some studies have indicated that the MWM task may be a more sensitive test for the effects of OPs on cognition. The hippocampus is considered to be an important region of the brain for learning and memory functions.49 It is known that hippocampus is involved in acquisition, retrieval, consolidation and storage of spatial memory. On the other hand, it is well established that hippocampal lesions affect the MWM performance.49 Our study showed that crocin effectively prevented malathion-induced loss of spatial memory impairment in rats (Figs. 1–3). In the present study, all of the experimental rats were trained during the acquisition experiments and had learned to locate the platform efficiently during the 5 days of training. Probe trials were carried out 48 h after the last day of training, in which the platform was removed from the pool. The latency to find the platform, swimming speed and distance swimming were recorded and used to evaluate spatial memory. After 2 weeks exposures, no differences were found in swimming speeds between all groups in both of tests. Malathion treated rats needed much more time to find the platform area (the former platform position) and spent less time and swim distance in the target quadrant compared with control group in the probe trials. Our findings showed that pretreatment with crocin (10 mg/kg) abolished the deleterious effects of malathion on learning and memory. These findings corroborate the previous studies demonstrate that low doses of crocin and saffron antagonized the destruction of recognition memory in the object recognition test and scopolamine-induced spatial memory performance deficits in the rat.39,50 We presumed the increased latency in MWM as a result of malathion exposure, was principal due to the impaired spatial memory. Our results are in agreement with another study that showed malathion (100 mg/kg) impaired spatial memory and discrimination, which was correlated with mitochondrial dysfunction, astrogliosis and apoptosis in hippocampus.51 It was also found that performance in a spatial learning task was impaired after 28 days of exposure to chlorpyrifos (1,5, and 10 mg/kg), another OP pesticide, through intragastric administration in rats.49 In another study, clothianidin, a neonicotinoid insecticide (2, 8 and 24 mg/kg) was administered to newborn infant and adult albino Wistar rats in the form of gavage. Data showed that exposure to high doses of clothianidin causes deterioration of cognitive functions in infant rats.47 In addition, exposure to other pesticides such as endosulfan (25 mg/kg) and methyl parathion (2 mg/kg) for 10 days or deltamethrin (12.5 mg/kg/day) and carbofuran (1 mg/kg/day) for 28 days indicated significantly longer escape latencies, higher number of failures to reach the platform and more time in the periphery of the tank than the control in MWM.52,53 These results are similar to our study.