Ecological risk assessment for aquatic invertebrate communities exposed to imidacloprid as a result of labeled agricultural and nonagricultural uses in the United States.

A probabilistic ecological risk assessment (ERA) was conducted to determine the potential effects of acute and chronic exposure of aquatic invertebrate communities to imidacloprid arising from labeled agricultural and nonagricultural uses in the United States. Aquatic exposure estimates were derived using a higher-tier refined modeling approach that accounts for realistic variability in environmental and agronomic factors. Toxicity was assessed using refined acute and chronic community-level effect metrics for aquatic invertebrates (i.e., species or taxon sensitivity distributions) developed using the best available data. Acute and chronic probabilistic risk estimates were derived by integrating the exposure distributions for different use patterns with the applicable species or taxon sensitivity distributions to generate risk curves, which plot cumulative probability of exceedance versus the magnitude of effect. Overall, the results of this assessment indicated that the aquatic invertebrate community is unlikely to be adversely affected by acute or chronic exposure to imidacloprid resulting from currently registered uses of imidacloprid in the United States. Environ Toxicol Chem 2017;36:1375-1388. © 2016 SETAC.

Disruption of the Class IIa HDAC Corepressor Complex Increases Energy Expenditure and Lipid Oxidation.

Drugs that recapitulate aspects of the exercise adaptive response have the potential to provide better treatment for diseases associated with physical inactivity. We previously observed reduced skeletal muscle class IIa HDAC (histone deacetylase) transcriptional repressive activity during exercise. Here, we find that exercise-like adaptations are induced by skeletal muscle expression of class IIa HDAC mutants that cannot form a corepressor complex. Adaptations include increased metabolic gene expression, mitochondrial capacity, and lipid oxidation. An existing HDAC inhibitor, Scriptaid, had similar phenotypic effects through disruption of the class IIa HDAC corepressor complex. Acute Scriptaid administration to mice increased the expression of metabolic genes, which required an intact class IIa HDAC corepressor complex. Chronic Scriptaid administration increased exercise capacity, whole-body energy expenditure and lipid oxidation, and reduced fasting blood lipids and glucose. Therefore, compounds that disrupt class IIa HDAC function could be used to enhance metabolic health in chronic diseases driven by physical inactivity.