Author: Connon, Richard E; Geist, Juergen; Pfeiff, Janice; Loguinov, Alexander V; D'Abronzo, Leandro S; Wintz, Henri; Vulpe, Christopher D; Werner, Inge
Title: Linking mechanistic and behavioral responses to sublethal esfenvalerate exposure in the endangered delta smelt; Hypomesus transpacificus (Fam. Osmeridae) Document date: 2009_12_15
ID: 1ecqnstz_46
Snippet: Microarray technology was used as an initial screening of probable genes responding to esfenvalerate exposure therefore no multiple testing correction was applied. We have, however, examined and confirmed effect of esfenvalerate upon some of the genes in a different age group of larval delta smelt, identifying significant responses that are primarily linked with swimming behavior. Some responding genes can be classified within different functiona.....
Document: Microarray technology was used as an initial screening of probable genes responding to esfenvalerate exposure therefore no multiple testing correction was applied. We have, however, examined and confirmed effect of esfenvalerate upon some of the genes in a different age group of larval delta smelt, identifying significant responses that are primarily linked with swimming behavior. Some responding genes can be classified within different functional groups. Due to the measured behavioral responses, the classification approach contains a certain bias towards understanding neuromuscular effects. It is interesting that qPCR measurements have identified a greater response at the lower concentrations, implying homeostatic alterations, at environmentally relevant concentrations. Most genes did not display a desired dose response correlation associated with usable biomarkers, but did support responses within the suite of genes investigated, somewhat validating their use within a broader biomarker approach. Hemopexin for example is known to be involved in axon repair, and the myelin sheath surrounding the axon needs to be degraded for this repair to be processed, hypothesizing therefore that ASPA downregulation is resultant of neurological damage. The subsequent decrease of hemopexin expression at higher exposure concentrations, and further decrease in ASPA, may be indicative of repair impairments.
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