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Acute Toxicity Testing by the Dermal Route
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
Roy C. Myers, Lin val R. DePass
A dramatic example of the effect of vehicle on dermal toxicity was reported by Brown and Muir.24 They found that rat dermal LD50s for the pesticide dicrotophos were approximately 20, 100, and 130 mg/kg when the respective vehicles were η-octanol, acetone, and isopropanol. These authors also demonstrated the effect of concentration on the toxicity of another pesticide (monocrotophos). The LD50s (based on active ingredient) were roughly 55 mg/kg with a 5% solution (in hexylene glycol), 95 mg/kg with a 10% solution, and 145 mg/kg with a 58% solution.
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
According to LD50 studies, which are accurate only for studies of acute exposures and, hence, invalid for approximating levels of chronic exposure, the order of descending toxicity for OPs (Figure 7.17) is tetraethyl pyrophosphate, phorate, disulfoton, fensulfothion, demeton, terbufor, meviphos, methidathion, chlormephos, sulfotep, chlorthiophos, monocrotophos, fonofos, prothoate, fenamiphos, phosfolan, methyl parathion, schradan, chlorfenvinphos, ethyl parathion, azinphos-methyl, phosphamidon, methamidophos, dicrotophos, isofenphos, bomy, carbophenothion, ethyl parathion (EPN), famphur, fenophosphon, dialifor, cyanofenphos, bromophos-ethyl, leopohos, dichlorvos, coumaphos, ethoprop, quinalphos, traizophos, demton-methyl, propetamphos, chlorpyrifos, sulprofos, dioxathion, isoxation, phosalone, thiometon, heptenophos, crotoxyphos, cythioate, phencapton, DEF, ethion, dimethoate, fenthion, dichlofenthion, and EPBP.144 Survival from these exposures can cause chemical sensitivity.
Female infertility caused by organophosphates: an insight into the latest biochemical and histomorphological findings
Published in Toxin Reviews, 2023
Mohammad Samare-Najaf, Ali Samareh, Bahia Namavar Jahromi, Navid Jamali, Sina Vakili, Majid Mohsenizadeh, Cain C. T. Clark, Ali Abbasi, Nastaran Khajehyar
Estrogen exerts its effects on tissues through two types of receptors, ER-α and ER-β. Interestingly, some OPs have agonistic effects on ER-α (e.g. butamifos) and ER-β (e.g. Prothiofos), while other OPs demonstrate antiandrogenic activity in CHO cells (e.g. fenitrothion, parathion, and methyl parathion). Importantly, some OPs have a selective performance and affect only one type of receptor. Butamifos, for instance, strongly stimulates ER-α while not having such an effect on ER-β (Κoφιµα, Κατσυρα ετ αλ. 2004). In addition to interfering with the interaction of E2 and its receptors, OPs have severe genotoxicity in CHO cells; for example, monocrotophos can cause chromosomal aberrations and reductions CHO cell proliferation through nucleophilic attack and DNA alkylation (Peitl et al.1996). Furthermore, dichlorvos, dicrotophos, malathion, parathion, and leptophos demonstrate antiproliferative properties via the induction of sister chromatid exchanges (Nishio and Uyeki 1981). Besides, exposure to OPs leads to cytogenotoxicity due to the induction of DNA double-strand breaks, suppression of mitochondrial activity, and threatens CHO cell viability (Patel et al.2007).