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Physiologically Based Pharmacokinetic Modeling to Predict Tissue Dose and Cholinesterase Inhibition in Workers Exposed to Organophosphorus and Carbamate Pesticides
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
James B. Knaak, Mohammed A. Al-Bayati, Otto G. Raabe
Knaak et al.12 showed that relatively small structural changes in isofenphos resulted in large changes in the partition coefficient and the chemical properties of the pesticide. Desulfuration of isofenphos to its oxon (P = S to P = O conversion) decreases its octanol-water partition coefficient from 25,000:1 to 600:1 (Log P 4.39 to 2.78), enhances its toxicity, and increases its rate of hydrolysis. The toxicity of parathion (paraoxon), malathion (malaoxon, 0,0-dimethyl S-[l,2-di(ethoxycarbonyl) ethyl] phosphorothioate) and several other OPs are also changed by desulfuration. The octanol/water partition coefficients for these compounds have not been reported.
Lindane and Malathion
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Jorg Heukelbach, Richard Speare, Essam S. Shaalan, Deon V. Canyon
Studies in humans have shown that chromosomal aberrations, sister chromatid exchanges, and mitotic indices were observed in human peripheral leukocytes treated in vitro with different concentrations (0.02, 0.2, 2, and 20 μg/ml) of malathion (Balaji and Sasikala, 1993). Zeljezic and Garaj-Vrhovac (2002) found that the mean value of sister chromatid exchange and number of cells with higher sister chromatid frequency in a population of workers occupationally exposed to a mixture of insecticides including malathion was significantly higher than in the control group. However, Titenko-Holland et al. (1997) concluded that malathion has a relatively low potential to cause chromosome damage in vitro, and that corresponding doses (5–100 μg/ml for 48 hours) are much higher than ones that even professional applicators of insecticides are likely to be exposed to in vivo. Consequently, the potential risk of chromosome damage for malathion exposure in vivo is therefore considered to be relatively low. In vitro studies of the genotoxicity of malathion and its analogs, malaoxon and isomalathion, indicated that malathion is a potential mutagen and carcinogen (Błasiak et al., 1999). The reported genotoxicity of malathion may be a consequence of its metabolic biotransformation to, or the presence of, malaoxon and/or isomalathion, as well as other unspecified impurities in commercial formulations of malathion.
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
Malathion [S-(1,2-dicarbethoxy) ethyl O,O-dimethyl phosphorodithioate] is one of the most widely employed OP pesticides for agriculture crops to control pests and public health programs. Malathion is a major cause of poisonings and deaths, mainly in developing countries. After enters the body, it is metabolized to malaoxon, a metabolite more harmful than malathion.12 Like other OPs, malathion could induce oxidative stress in different tissues in long term exposure.13 Toxic effects of malathion have been widely studied in experimental animals and in exposed workers.14 It has been indicated that malathion exposure increased lipid peroxidation in the erythrocytes, liver, and brain of rats. Moreover, the lipophilic nature of malathion facilitates its interaction with the mitochondrial membrane and leads to release of cytochrome c which may initiate apoptosis of exposed cells.15 Recently, it has been demonstrated the neuronal cell loss associated with AD may be mediated via the process of apoptosis.16 It has also suggested the induction of apoptosis may be as a result of repeated organophosphate exposure.17
Evaluation on the thyroid disrupting mechanism of malathion in Fischer rat thyroid follicular cell line FRTL-5
Published in Drug and Chemical Toxicology, 2018
Jingyuan Xiong, Liantian Tian, Yongjie Qiu, Ding Sun, Hao Zhang, Mei Wu, Jintao Wang
Although malathion is believed to mainly target insects and considered safe for its low human exposure, it can be readily converted to toxic malaoxon after inhalation, ingestion, and absorption by mammals (Morgade and Barquet 1982, Marty et al. 1994). Postnatal studies in mice reported that malathion significantly inhibited brain acetylcholinesterase activity in the offspring’s (Mortensen et al. 1998, Selmi et al. 2012). In human studies, malathion was shown to markedly affect acetylcholinesterase activity when given at a high dosage for 56 consecutive days, suggesting possible interferences with mammalian cerebral development (Moeller and Rider 1962, HHS 2008). Therefore, pregnant women are susceptible to malathion since neuronal growth and cellular differentiation in central nervous system of fetus are crucial developments during pregnancy (Nicholson and Altman 1972, Lavado-Autric et al. 2003, Auso et al. 2004, Zoeller and Rovet 2004). While there is no doubt that malaoxon acts on acetylcholinesterase, but further verification is required whether malathion directly affects thyroid hormone system.