• Corpus ID: 88179971

Pode a exposição humana ao inseticida clorpirifós alterar o desenvolvimento do sistema nervoso central? Contribuições de experimentos em animais

@inproceedings{Meyer2005PodeAE,
  title={Pode a exposiç{\~a}o humana ao inseticida clorpirif{\'o}s alterar o desenvolvimento do sistema nervoso central? Contribuiç{\~o}es de experimentos em animais},
  author={Armando Meyer},
  year={2005}
}
There is increasing evidence that the mechanism for systemic toxicity, named cholinergic hyperstimulation consequent to inhibition of cholinesterase, is not the primary mechanism for adverse effects of chlorpyrifos (CPF) during development. In fact, many studies have shown that CPF disrupts the fundamental processes of brain development. In addition, neonatal exposure to CPF alters cell signaling mediated by adenylyl cyclase, the enzyme responsible for cyclic AMP production, a major… 
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The objective of this study is to demonstrate the use of infrared thermography in a geoscience context to diagnose thermal and hydrological patterns in soils with crops irrigated using clay pots in

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Developmental neurotoxicity elicited by gestational exposure to chlorpyrifos: when is adenylyl cyclase a target?

Results indicate that signal transduction through the AC cascade is a target for CPF during a discrete developmental period in late gestation, an effect that is likely to contribute to the noncholinergic component of CPF's developmental neurotoxicity.

Serotonergic systems targeted by developmental exposure to chlorpyrifos: effects during different critical periods.

The results indicate that CPF affects 5HT receptors, the presynaptic 5HT transporter, and 5HT-mediated signal transduction during a discrete critical gestational window, which is likely to contribute to the noncholinergic component of CPF's developmental neurotoxicity.

Fetal chlorpyrifos exposure: adverse effects on brain cell development and cholinergic biomarkers emerge postnatally and continue into adolescence and adulthood.

A wide window of vulnerability of cholinergic systems to CPF is indicated, extending from prenatal through postnatal periods, occurring independently of adverse effects on general cellular neurotoxicity.

Age-related effects of chlorpyrifos on muscarinic receptor-mediated signaling in rat cortex

The results provide further evidence that the cortical cAMP signaling pathway may be particularly sensitive to CPF exposure in neonatal, juvenile, and adult rats, possibly due to a direct interaction between CPF (or its oxon) and mAChRs or other components of the adenylyl cyclase cascade.

Developmental exposure to chlorpyrifos elicits sex-selective alterations of serotonergic synaptic function in adulthood: critical periods and regional selectivity for effects on the serotonin transporter, receptor subtypes, and cell signaling.

The results indicate that CPF elicits long-lasting changes in 5HT receptors, the presynaptic 5HT transporter, and 5HT-mediated signal transduction after exposure in discrete developmental windows that range from the neural tube stage through synaptogenesis.

Developmental neurotoxicity elicited by prenatal or postnatal chlorpyrifos exposure: effects on neurospecific proteins indicate changing vulnerabilities.

The results indicate a shift in the populations of neural cells targeted by CPF, dependent upon the period of exposure, and developmental differences in the sex selectivity of the biochemical mechanisms underlying neurotoxicant actions are likely to contribute to discrete behavioral outcomes.
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