2013
DOI: 10.1016/j.tox.2013.04.007
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The molecular basis of simple relationships between exposure concentration and toxic effects with time

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Cited by 94 publications
(69 citation statements)
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References 97 publications
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“…The neuronal death toll accumulates as more and more pesticide molecules bind to other nAChRs until the organism cannot cope with the damage and dies. The main difference between this mode of action and that of other pesticides is that effects are cumulative with time, because neurons do not regenerate-it has been termed time-cumulative or reinforced toxicity (Tennekes and Sánchez-Bayo 2013). This mechanism certainly applies to all arthropods tested to date, but not to birds.…”
Section: The Delayed Mortality and Chronic Toxicity Of Neonicotinoidsmentioning
confidence: 99%
“…The neuronal death toll accumulates as more and more pesticide molecules bind to other nAChRs until the organism cannot cope with the damage and dies. The main difference between this mode of action and that of other pesticides is that effects are cumulative with time, because neurons do not regenerate-it has been termed time-cumulative or reinforced toxicity (Tennekes and Sánchez-Bayo 2013). This mechanism certainly applies to all arthropods tested to date, but not to birds.…”
Section: The Delayed Mortality and Chronic Toxicity Of Neonicotinoidsmentioning
confidence: 99%
“…Delayed mortality, also called time-cumulative toxicity or reinforced toxicity, results in increased mortality rates with time of exposure and it applies to toxicants that act irreversibly or slowly reversibly on a receptor while producing an irreversible effect [63]. It can be detected by estimating the acute/chronic ratios of a toxic substance, which in this case may span two or three orders of magnitude [64], but the best way to assess it is by conducting time-to-event (TTE) toxicity tests.…”
Section: Toxicity Assessmentmentioning
confidence: 99%
“…If the cell cannot be regenerated (i.e. neurons), such an effect is irreversible, hence the resulting pattern of toxicity is not only dependent on dose but also on the time of exposure to sublethal levels [63]. For such chemicals, the risk assessment should aim at determining the time to 50% mortality (T50) in a population under the normal and worst exposure scenarios, as it has been described elsewhere [28].…”
Section: Risk Assessmentmentioning
confidence: 99%
“…It is a relatively new pesticide (patent 1985) 1 , which is a disruptor of the nervous system by acting as an inhibitor at nicotinic acetylcholine receptors found in many insects 2 . The possible relationship between neonicotinoid pesticides and massive disappearance of honeybees from the hive is a topic of great interest nowadays [3][4] .…”
Section: Introductionmentioning
confidence: 99%