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Organophosphorus Compound-Induced Mitochondrial Disruption
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Research into the biochemical basis of OPIDN has shown that certain molecular events occur within 24 hours of exposure, thus preceding the onset of clinical signs. The first of these molecular lesions is the inhibition and aging of neuropathy target esterase (NTE) which, like AChE is a member of the serine esterase family; this is the main molecular initiating event in OPIDN (Johnson, 1974, 1982, 1990; Bal-Price et al., 2015). However, it may not be the serine esterase activity per se, which is responsible for triggering OPIDN, as NTE is now known to exhibit several other biochemical properties such as phospholipase and ion channel activities whose disruption may contribute to the development of the neuropathy (Glynn, 1999a, 1999b, 2000, 2005). A second major biochemical lesion detected in animal models of OPIDN and in cellular models of OP-induced neurite disruption are increased phosphorylation and increased degradation of cytoskeletal proteins (Suwita et al., 1986; Zhao et al., 2004).
Neurotoxicity of Pesticides
Published in Ana Maria Osorio, Lynn R. Goldman, Proceedings from the Medical Workshop on Pesticide-Related Illnesses from the International Conference on Pesticide Exposure and Health, 2017
Matthew C. Keifer, Jordan Firestone
One of the most intriguing presentations of chronic pesticide related illness is organophosphate induced delayed polyneuropathy (OPIDP). This predominantly motor neuropathy can occur with only a handful of organophosphates.53,54 An organophosphate's ability to induce OPIDP appears to depend on its ability to inhibit a neuron membrane-associated protein known as neuropathy target esterase.55.56 OPIDP is usually heralded by the onset of pain and cramping of the lower extremities beginning around two weeks after acute organophosphate intoxication. Sensory changes are generally minor, but motor dysfunction may be severe, characterized by a progressive, ascending, flaccid paralysis which may be only partially reversible. Cases of OPIDP following triortho-cresyl-phosphate poisoning suggest that concomitant, myelopathic effects with spastic weakness may complicate assessment of the most severely affected individuals.
Determination
Published in David Woolley, Adam Woolley, Practical Toxicology, 2017
In the blood, measurement of cholinesterases may indicate toxicity due to organophosphate or carbamate pesticides; however, after chronic administration, rats can show large decreases in activity without clinical evidence of effect. Organophosphates, which inhibit cholinesterases (as do carbamates), are classically associated with delayed-onset neuropathy, which has been tested routinely in chickens. This has been the species of choice for assessment of the target enzyme for this condition, neuropathy target esterase. Much emphasis is placed on histopathology, where the use of special fixatives and stains with appropriate microscopic technique can be very informative.
Oliver McFarlane syndrome: two new cases and a review of the literature
Published in Ophthalmic Genetics, 2021
Kristian Lisbjerg, Mette K. G. Andersen, Mette Bertelsen, Agnes G. Brost, Frederik F. Buchvald, Rikke B. Jensen, Anne-Marie Bisgaard, Thomas Rosenberg, Zeynep Tümer, Line Kessel
Genetic testing of patients with Oliver McFarlane syndrome places this condition within the spectrum of PNPLA6-associated disorders. Abnormalities in the phospholipids levels has been documented in PNPLA6 mutant drosophila flies and in patients and carriers of PNPLA6 variants (5). Patients with retinal manifestations more often carries at least one PNPLA6-variant in the patatin-like phospholipase domain (pat domain) (10). PNPLA6 is expressed in developing and mature mouse retina in the inner segment plasma membrane of photoreceptors (5) and accumulation of phospholipids can lead to photoreceptor degeneration (25). In neuropathy target esterase (NTE) deficient mice increased phosphatidylcholine in the brain caused degeneration of long axons leading to spinocerebellar features (26). Furthermore, a diminished LH response to gonadotropin releasing hormone was seen after NTE activity inhibition in the gonadotrope cell line which may explain the hypogonadotropic hypogonadism seen in carriers of PNPLA6 variants (27). Other anterior pituitary hormone deficiencies are well described in these disorders, but no clear pathophysiology have been clarified. The characteristic trichomegaly in Oliver McFarlane syndrome may result from increased prostaglandin formation due to increased phosphatidylethanolamine in follicular cells as prostaglandins play important roles in hair homeostasis (28).
Advances in detection of hazardous organophosphorus compounds using organophosphorus hydrolase based biosensors
Published in Critical Reviews in Toxicology, 2019
Monika Jain, Priyanka Yadav, Abhijeet Joshi, Prashant Kodgire
OP-induced delayed polyneuropathy is also a severe toxic effect of OPs exerted on the central nervous system and peripheral nervous system. The root cause of this neuropathy is the modification and phosphorylation of the neuropathy target esterase enzyme in the central nervous system. An increase in autophosphorylation has been observed in the calmodulin kinases due to the presence of OPs. This increases the phosphorylation of cytoskeletal proteins, such as myelin basic protein, α and β tubulin, neurofilament protein, microtubule-associated protein-2. Consequently, the transport rate of cytoskeletal protein is decreased down the axon compared to their entry rate resulting in their accumulation in the distal part of the axon. Thus, the delayed OP-induced polyneuropathy is marked by bulging in the axons of the central and peripheral nervous system with subsequent ataxia and paralysis (Abou-Donia 1995).
Effect of pesticide exposure on the cholinesterase activity of the occupationally exposed tea garden workers of northern part of West Bengal, India
Published in Biomarkers, 2019
OP and carbamate pesticides exert their toxic effects through inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine at peripheral and central cholinergic receptors, leading to the overstimulation of the cholinergic system (Altuntas et al. 2002, Rendón von Osten et al. 2004, Cataño et al. 2008) and subsequent paralysis. The butyrylcholinesterase (BuChE) also known as pseudocholinesterase, abundant in plasma, liver, smooth muscle and fat cells (Simoniello et al. 2010) can bind covalently to OP and carbamates. Other serine esterases such as carboxylesterase (CaE), neuropathy target esterase (NTE) and trypsin as well as chymotrypsin also have affinity to OPs (Worek et al. 2005). A number of clinical symptoms like nausea, vomiting, rhinorrhea, anxiety, somnolence, gait disturbance, sleep disturbance, abdominal pain, headache, dizziness, irritability, fatigue, limb pain, limb numbness, paresthesias and limb weakness have already been shown to manifest due to chronic OP toxicity (Ecobichon 1996, Karalliedde 1999). Therefore, several studies have indicated AChE and BuChE as an effective biomarker for monitoring OP and carbamate exposure (Chakraborty et al. 2009, Simoniello et al. 2010, Kapka-Skrzypczak et al. 2011, Krenz et al. 2014, Guytingco et al. 2018).