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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
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.
An Overview of the NIAID/NIH Chemical Medical Countermeasures Product Research and Development Program *
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
David. T. Yeung, Gennady. E. Platoff Jr., Jill. R. Harper, David. A. Jett
A number of the chemical threats of interest are known to primarily target the nervous system. These chemicals include cholinergic agents that can induce seizures potentially followed by neuropathology and in the longer term, adverse neurological sequelae. The biological and mechanistic details of the injury processes are described elsewhere in this book and will not be discussed here in-depth. From the civilian perspective, cholinergic-based chemical threats specifically include the classical CWA nerve agents as well as OP pesticides such as chlorpyrifos, phorate, paraoxon, and disulfoton. Included here as well are the carbamate pesticides, such as aldicarb and methomyl. The primary mechanism of toxicity exerted by OP and carbamate poisons is anti-cholinesterase (anti-ChE) activity via inhibition of ChE enzymes, especially the neurotransmitter acetylcholinesterase (AChE). The inhibition of AChE results in increased acetylcholine (ACh) levels in the synapses of central and peripheral nervous systems. If this increase is left uncontrolled, clinical manifestations of intoxication such as miosis, fasciculations, respiratory distress, seizures, convulsions, increased secretions, and death can quickly occur (Bajgar, 2004, 2005; Taylor, 2001). While the mechanism of toxicity via cholinergic hyperstimulation is the same for the CWAs and carbamate and OP pesticides, the relative potencies can be radically different (Hollingshaus et al., 1983; Parker and Goldstein, 2000). To date, the NIH has supported numerous projects aimed at mitigating cholinergic toxicity. These various projects have taken a number of different antidotal and symptom-based therapeutic approaches.
Impacts of ingested MWCNT-Embedded nanocomposites in Japanese medaka (Oryzias latipes)
Published in Nanotoxicology, 2021
Melissa Chernick, Alan Kennedy, Treye Thomas, Keana C. K. Scott, Christine Ogilvie Hendren, Mark R. Wiesner, David E. Hinton
Striking were the relatively large areas of degenerated cells observed in fish exposed to abraded nanocomposites. This finding supports hepatocellular alterations observed in histologic sections of the liver. The transformation of RER into highly condensed myelin-like figures that we observed is illustrative of progressive toxic action by these materials, an effect also observed by Arnold et al. (1996) with disulfoton exposures to rainbow trout (Oncorhynchus mykiss). The type of lethal hepatocellular injury observed in these livers could have been due to the breakdown of the plasma membrane following penetration or intracellular accumulation of toxins in the cell (Popper 1988) and/or lipid peroxidation due to ROS (Ekström and Ingelman-Sundberg 1986). The remaining hepatocytes appeared to have lost volume control indicating that cells had lost regulatory mechanisms that preserve membrane integrity (Chara et al. 2011), supporting this hypothesis. Oxidative stress or direct physical interference with cellular- (e.g. actin cytoskeleton, mitotic spindles) and extracellular constituents resulting in non-oxidative stress-mediated cellular damage are also possible underlying mechanisms for the effects we observed in the present study (Shvedova et al. 2012). Future studies will be needed to determine if they are occurring with these materials. As we did not observe damage to this extent with either pristine material, this may be a unique mixture effect.
Adrenaline is effective in reversing the inadequate heart rate response in atropine treated organophosphorus and carbamate poisoning
Published in Clinical Toxicology, 2021
Abhishek Samprathi, Binila Chacko, Shilpa Reynal D’sa, Grace Rebekah, C. Vignesh Kumar, Mohammad Sadiq, Punitha Victor, John Prasad, Jonathan Arul Jeevan Jayakaran, John Victor Peter
Persistence of acetylcholine receptor blockade can be either due to secondary blockade of receptors or receptor desensitization [20]. In animal studies, the enhanced potency of parathion-ethyl and disulfoton at elevated acetylcholine concentration was shown to be due to a persistently blocked, desensitized state [20]. In another study, Soman and echothiophate in micromolar concentrations acted as partial agonists of the n-ACh receptor and induced receptor desensitization [21]. Although this phenomenon has so far been demonstrated only in the nicotinic ACh receptors which are linked to ion channels (ionotropic receptors) where atropine would be ineffective, it is possible that similar changes may also occur in muscarinic receptors which use G-proteins as the signaling mechanism (metabotropic receptors). If such a mechanism was in play in muscarinic receptors, then a desensitized receptor state could perpetuate the low HR in OP poisoning.
Functional assessment of rat pulmonary flavin-containing monooxygenase activity
Published in Xenobiotica, 2019
Yildiz Yilmaz, Gareth Williams, Nenad Manevski, Markus Walles, Stephan Krähenbühl, Gian Camenisch
The flavin-containing monooxygenases (FMOs) are a family of enzymes that typically catalyze the oxygenation of substrates containing a soft nucleophilic heteroatom such as nitrogen or sulfur. Human FMO5 has recently also been shown to behave as a Baeyer–Villiger monooxygenase, catalyzing the conversion of a lactone or ketone to an ester (Fiorentini et al., 2017; Lai et al., 2010; Meng et al., 2015). In humans, the FMO family is relatively small and only five functional genes (FMO1–5) have been identified (Lawton et al., 1994; Phillips et al., 1995). FMO substrates include dietary compounds, insecticides and drugs such as trimethylamine (Dolphin et al., 1997), phorate and disulfoton (Henderson et al., 2004), imipramine (Furnes & Schlenk, 2004), clozapine (Tugnait et al., 1997) and ethionamide (Henderson et al., 2008).