PMID- 22579662 OWN - NLM STAT- MEDLINE DCOM- 20121102 LR - 20131121 IS - 1532-0456 (Print) IS - 1532-0456 (Linking) VI - 156 IP - 2 DP - 2012 Aug TI - Temporal changes in stress and tissue-specific metabolic responses to municipal wastewater effluent exposure in rainbow trout. PG - 67-74 LID - 10.1016/j.cbpc.2012.04.002 [doi] AB - Sub-chronic exposure to municipal wastewater effluent (MWWE) in situ was recently shown to impact the acute response to a secondary stressor in rainbow trout (Oncorhynchus mykiss). However, little is known about whether MWWE exposure in itself is stressful to the animal. To address this, we carried out a laboratory study to examine the organismal and cellular stress responses and tissue-specific metabolic capacity in trout exposed to MWWE. Juvenile rainbow trout were exposed to 0, 20 and 90% MWWE (from a tertiary wastewater treatment plant), that was replenished every 2d, for 14 d. Fish were sampled 2, 8 or 14 d post-exposure. Plasma cortisol, glucose and lactate levels were measured as indicators of organismal stress response, while inducible heat shock protein 70 (hsp70), constitutive heat shock protein 70 (hsc70) and hsp90 expression in the liver were used as markers of cellular stress response. Impact of MWWE on cortisol signaling was ascertained by determining glucocorticoid receptor protein (GR) expression in the liver, brain and, heart, and metabolic capacity was evaluated by measuring liver glycogen content and tissue-specific activities of key enzymes in intermediary metabolism. Plasma glucose and lactate levels were unaffected by exposure to MWWEs, whereas cortisol showed a transient increase in the 20% group at 8d. Liver hsc70 and hsp90, but not hsp70 expression, were higher in the 90% MWWE group after 8d. There was a temporal change in GR expression in the liver and heart, but not brain of trout exposed to MWWE. Liver glycogen content and activities liver gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK), and alanine aminotransferase (AlaAT) were significantly affected by MWWE exposure. The glycolytic enzymes pyruvate kinase (PK) and hexokinase (HK) activities were significantly higher temporally by MWWE exposure in the gill and heart, but not in the liver and brain. Overall, a 14 d exposure to MWWE evokes a cellular stress response and perturbs the cortisol stress response in rainbow trout. The tissue-specific temporal changes in the metabolic capacity suggest enhanced energy demand in fish exposed to MWWE, which may eventually lead to reduced fitness. CI - Copyright (c) 2012 Elsevier Inc. All rights reserved. FAU - Ings, Jennifer S AU - Ings JS AD - Department of Biology, University of Waterloo, Ontario, Canada. FAU - Oakes, Ken D AU - Oakes KD FAU - Vijayan, Mathilakath M AU - Vijayan MM FAU - Servos, Mark R AU - Servos MR LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120501 PL - United States TA - Comp Biochem Physiol C Toxicol Pharmacol JT - Comparative biochemistry and physiology. Toxicology & pharmacology : CBP JID - 100959500 RN - 0 (Blood Glucose) RN - 0 (HSP70 Heat-Shock Proteins) RN - 0 (HSP90 Heat-Shock Proteins) RN - 0 (Liver Glycogen) RN - 0 (Receptors, Glucocorticoid) RN - 0 (Water Pollutants, Chemical) RN - 33X04XA5AT (Lactic Acid) RN - EC 2.7.1.40 (Pyruvate Kinase) RN - EC 4.1.1.49 (Phosphoenolpyruvate Carboxykinase (ATP)) RN - WI4X0X7BPJ (Hydrocortisone) SB - IM MH - Animals MH - Blood Glucose/analysis/metabolism MH - Brain/drug effects/metabolism MH - Carbohydrate Metabolism MH - Environmental Exposure/*analysis MH - Enzyme Activation MH - Gills/drug effects/metabolism MH - HSP70 Heat-Shock Proteins/analysis/metabolism MH - HSP90 Heat-Shock Proteins/metabolism MH - Hydrocortisone/blood MH - Lactic Acid/metabolism MH - Liver/drug effects/metabolism MH - Liver Glycogen/analysis MH - Oncorhynchus mykiss/*metabolism MH - Phosphoenolpyruvate Carboxykinase (ATP)/metabolism MH - Pyruvate Kinase/metabolism MH - Receptors, Glucocorticoid/metabolism MH - *Stress, Physiological MH - Water Pollutants, Chemical/*toxicity EDAT- 2012/05/15 06:00 MHDA- 2012/11/03 06:00 CRDT- 2012/05/15 06:00 PHST- 2011/10/05 00:00 [received] PHST- 2012/04/17 00:00 [revised] PHST- 2012/04/17 00:00 [accepted] PHST- 2012/05/15 06:00 [entrez] PHST- 2012/05/15 06:00 [pubmed] PHST- 2012/11/03 06:00 [medline] AID - S1532-0456(12)00057-9 [pii] AID - 10.1016/j.cbpc.2012.04.002 [doi] PST - ppublish SO - Comp Biochem Physiol C Toxicol Pharmacol. 2012 Aug;156(2):67-74. doi: 10.1016/j.cbpc.2012.04.002. Epub 2012 May 1.