Mechanisms for consideration for intervention in the development of organophosphorus-induced delayed neuropathy

Emerick, Guilherme Luz; DeOliveira, Georgino H.; Santos, Antônio Cardozo dos; Ehrich, Marion

doi:10.1016/j.cbi.2012.07.002

Cited by 35 publications

(19 citation statements)

References 68 publications

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“…In vivo (hens) and in vitro (SH-SY5Y cells) studies have associated the axonal degeneration following the exposure to neuropathic OPs with excessive influx of calcium and activation of calcium-dependent proteases, also known as calpains (el-Fawal et al, 1990;Choudhary and Gill, 2001;Choudhary et al, 2006;Emerick et al, 2012a). Mipafox, which is known as inducer of OPIDN, and trichlorfon were able to significantly increase the intracellular calcium levels after 24 h of exposure.…”

Section: Discussionmentioning

confidence: 97%

“…Although inhibition of acetylcholinesterase (AChE) plays a key role in the toxicity of OPs, this mechanism does not explain the delayed neuropathy induced by some OPs (Johnson, 1975b;Liu et al, 2009;Emerick et al, 2012a;Terry, 2012b). OPIDN inducers differ from OPs that induce acute toxicity in their potency to inhibit AChE and NTE (neuropathy target esterase) (Cho and TiffanyCastiglioni, 2004).…”

Section: Introductionmentioning

confidence: 98%

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In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

Fernandes

Emerick

Santos

et al. 2015

Toxicology in Vitro

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

Fernandes

Emerick

Santos

et al. 2015

Toxicology in Vitro

Self Cite

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“…On the other hand, adult mice seem to 1497 be resistant to similar insults (Veronesi et al, 1991) and present 1498 axonal degeneration and paralysis only after long exposure up to 1499 9 months to these compounds (Lapadula et al, 1985). 1500 This AOP has as a MIE the binding of OPIDN inducers to NTE, (Emerick et al, 2012). In 1539 an experimental study, co-exposure of rats to a Ca 2+ channel 1540 blocker and dichlorvos prevented neurobehavioral alterations 1541 induced by dichlorvos but no prevention of NTE inhibition has 1542 been found (Choudhary and Gill, 2001 (Choudhary and Gill, 2001).…”

mentioning

confidence: 98%

Increasing Scientific Confidence in Adverse Outcome Pathways: Application of Tailored Bradford-Hill Considerations for Evaluating Weight of Evidence

Becker

Ankley

Edwards

et al. 2015

Regulatory Toxicology and Pharmacology

213

198

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Systematic consideration of scientific support is a critical element in developing and, ultimately, using adverse outcome pathways (AOPs) for various regulatory applications. Though weight of evidence (WoE) analysis has been proposed as a basis for assessment of the maturity and level of confidence in an AOP, methodologies and tools are still being formalized. The Organization for Economic Co-operation and Development (OECD) Users' Handbook Supplement to the Guidance Document for Developing and Assessing AOPs (OECD 2014a; hereafter referred to as the OECD AOP Handbook) provides tailored Bradford-Hill (BH) considerations for systematic assessment of confidence in a given AOP. These considerations include (1) biological plausibility and (2) empirical support (dose-response, temporality, and incidence) for Key Event Relationships (KERs), and (3) essentiality of key events (KEs). Here, we test the application of these tailored BH considerations and the guidance outlined in the OECD AOP Handbook using a number of case examples to increase experience in more transparently documenting rationales for assigned levels of confidence to KEs and KERs, and to promote consistency in evaluation within and across AOPs. The major lessons learned from experience are documented, and taken together with the case examples, should contribute to better common understanding of the nature and form of documentation required to increase confidence in the application of AOPs for specific uses. Based on the tailored BH considerations and defining questions, a prototype quantitative model for assessing the WoE of an AOP using tools of multi-criteria decision analysis (MCDA) is described. The applicability of the approach is also demonstrated using the case example aromatase inhibition leading to reproductive dysfunction in fish. Following the acquisition of additional experience in the development and assessment of AOPs, further refinement of parameterization of the model through expert elicitation is recommended. Overall, the application of quantitative WoE approaches hold promise to enhance the rigor, transparency and reproducibility for AOP WoE determinations and may play an important role in delineating areas where research would have the greatest impact on improving the overall confidence in the AOP.

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“…Although all of them can bind to acetylcholine esterase at nerve terminals, each of them might have different additional targets and target organs. For instance, only a subgroup affects neuropathy target esterase and causes delayed neuropathy (Emerick et al 2012;Ehrich et al 1997). Some organophosphates may be involved in inflammation or inflammatory diseases such as asthma (Proskocil et al 2013;Banks and Lein 2012).…”

mentioning

confidence: 99%

Monocrotophos in Gandaman village: India school lunch deaths and need for improved toxicity testing

et al. 2013

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Mechanisms for consideration for intervention in the development of organophosphorus-induced delayed neuropathy

Cited by 35 publications

References 68 publications

In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

Increasing Scientific Confidence in Adverse Outcome Pathways: Application of Tailored Bradford-Hill Considerations for Evaluating Weight of Evidence

Monocrotophos in Gandaman village: India school lunch deaths and need for improved toxicity testing

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