1. The mechanism of the anti-nutritive activities of soluble non-starch polysaccharides (NSPs) in broiler diets was investigated with emphasis on the inter-relationship between viscosity and fermentation along the gut. Isolated soluble NSP were added to a control diet to effect high gut viscosity, and in vivo depolymerisation of the NSP was achieved using a commercial glycanase. 2. Addition of soluble NSPs significantly (P < 0.01) increased gut viscosity, reduced the AME of the diet and depressed the growth and FCE of the birds. Enzyme supplementation of the NSP-enriched diet reversed the adverse effects, increasing (P < 0.01) weight gain, FCE and AME. Comparisons of the viscosities (mPa) in birds fed on the NSP-enriched diet and the same diet supplemented with enzyme were respectively: 11.9 v. 2.3 in the duodenum; 78.3 v. 4.4 in the jejunum and 409.3 v. 10.8 in the ileum. 3. Caecal volatile fatty acid concentration was markedly (P < 0.01) elevated by enzyme supplementation, whereas ileal fermentation was inhibited. 4. Microscopic examination revealed that, among birds fed on the NSP-enriched diet, there had been extensive small intestinal fermentation, which was eliminated by the enzyme supplementation. 5. Addition of a synthetic antibiotic (Amoxil) had no beneficial effects. 6. The current study demonstrated that increased fermentation occurs in the small intestine when a large amount of viscous NSPs is present in the diet and this is detrimental to the performance and well-being of poultry.

BackgroundNew methods are needed for research into non-model organisms, to monitor the effects of toxic disruption at both the molecular and functional organism level. We exposed earthworms (Lumbricus rubellus Hoffmeister) to sub-lethal levels of copper (10–480 mg/kg soil) for 70 days as a real-world situation, and monitored both molecular (cDNA transcript microarrays and nuclear magnetic resonance-based metabolic profiling: metabolomics) and ecological/functional endpoints (reproduction rate and weight change, which have direct relevance to population-level impacts).ResultsBoth of the molecular endpoints, metabolomics and transcriptomics, were highly sensitive, with clear copper-induced differences even at levels below those that caused a reduction in reproductive parameters. The microarray and metabolomic data provided evidence that the copper exposure led to a disruption of energy metabolism: transcripts of enzymes from oxidative phosphorylation were significantly over-represented, and increases in transcripts of carbohydrate metabolising enzymes (maltase-glucoamylase, mannosidase) had corresponding decreases in small-molecule metabolites (glucose, mannose). Treating both enzymes and metabolites as functional cohorts led to clear inferences about changes in energetic metabolism (carbohydrate use and oxidative phosphorylation), which would not have been possible by taking a 'biomarker' approach to data analysis.ConclusionMultiple post-genomic techniques can be combined to provide mechanistic information about the toxic effects of chemical contaminants, even for non-model organisms with few additional mechanistic toxicological data. With 70-day no-observed-effect and lowest-observed-effect concentrations (NOEC and LOEC) of 10 and 40 mg kg-1 for metabolomic and microarray profiles, copper is shown to interfere with energy metabolism in an important soil organism at an ecologically and functionally relevant level.

Risk assessment of metal-contaminated habitats based on responses in the field is complicated by the evolution of local, metal-resistant ecotypes. The unpredictability of occurrence of genetically determined adaptive traits, in terms of site-specific geochemistry, a population's inferred exposure history, and in the physiology of resistance, exacerbates the problem. Micro-evolutionary events warrant the attention of ecotoxicologists because they undermine the application of the bedrock of toxicology, the dose-response curve, to in situ field assessments. Here we survey the evidence for the existence of genetically differentiated, metal-resistant, invertebrate populations; we also describe some of the molecular mechanisms underpinning the adaptations. Quantitative changes in tissue-metal partitioning, and in the molecular and cellular responses (biomarkers)to alterations in internal bioreactive metal pools, are widely accepted as indicators of toxicity and/or exposure in free-living organisms. Both can be modulated by resistance. The understanding that all genomes are intrinsicallyflexible, with subtle sequence changes in promoter regions or epigenetic adjustments conferring significant phenotypic consequences, is deemed highly relevant. Equally relevant is the systems biology insight that genes and proteins are woven into networks. We advocate that biomarker studies should work toward assimilating and exploiting these biological realities through monitoring the activities of suites of genes (transcriptomics) and their expressed products (proteomics), as well as profiling the metabolite signatures of individuals (metabolomics) and by using neutral genetic markers to genotype populations. Ecotoxicology requires robust tools that recognize the imprint of evolution on the constitution of field populations, as well as sufficient mechanistic understanding of the molecular-genetic observations to interpret them in meaningful environmental diagnostic ways.

Stress-activated protein kinases (SAPKs), consisting of c-Jun N-terminal kinase (JNK) and p38 mitogenactivated protein kinase (p38 MAPK), are activated upon various environmental stimuli, including viral infections. Cellular survival and death signaling events following coxsackievirus B3 (CVB3) infection have been studied in relationship to viral replication, but the role of SAPKs has not been scrutinized. In this study, we found that the phosphorylation of JNK1