Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to investigate the impact of short-term exposure to polychlorinated biphenyls on the acute stress response in rainbow trout. Fish were exposed to dietary Aroclor1254 (10mg kg(-1) body mass/day) for 3 days and then subjected to a 3-min handling disturbance and sampled over a 24h recovery after the stressor exposure. In the pre-stress fish, PCB exposure significantly elevated aryl hydrocarbon receptor (AhR) and cytochrome P4501A1 (Cyp1A1) mRNA abundance and Cyp1A protein expression confirming AhR activation. There was no significant effect of PCB on plasma cortisol and glucose levels, while plasma lactate levels were significantly elevated compared to the sham group. PCB exposure significantly elevated liver glycogen content and hexokinase activity, whereas lactate dehydrogenase activity was depressed. Short-term PCB exposure did not modify the acute stressor-induced plasma cortisol, glucose and lactate responses. Liver glycogen content dropped significantly after stressor exposure in the PCB group but not in the sham group. This was matched by a significantly higher liver LDH activity and a lower HK activity during recovery in the PCB group suggesting enhanced glycolytic capacity to fuel hepatic metabolism. Liver AhR, but not Cyp1A1, transcript levels were significantly reduced during recovery from handling stressor in the Aroclor fed fish. Collectively, this study demonstrates that short-term PCB exposure may impair the liver metabolic performance that is critical to cope with the enhanced energy demand associated with additional stressor exposure in rainbow trout.
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PMID:Aroclor 1254 disrupts liver glycogen metabolism and enhances acute stressor-mediated glycogenolysis in rainbow trout. 2174 95

The skin is constantly exposed to a variety of environmental threats, including solar electromagnetic radiation, microbes, airborne particulate matter, and chemicals. Acute exposure to these environmental factors results in the activation of different signaling pathways that orchestrate adaptive stress responses to maintain cell and tissue homeostasis. Chronic exposure of skin to these factors, however, may lead to the accumulation of damaged macromolecules and loss of cell and tissue integrity, which, over time, may facilitate aging processes and the development of aging-related malignancies. One transcription factor that is expressed in all cutaneous cells and activated by various environmental stressors, including dioxins, polycyclic aromatic hydrocarbons, and ultraviolet radiation, is the aryl hydrocarbon receptor (AHR). By regulating keratinocyte proliferation and differentiation, epidermal barrier function, melanogenesis, and immunity, a certain degree of AHR activity is critical to maintain skin integrity and to adapt to acute stress situations. In contrast, a chronic activation of cutaneous AHR signaling critically contributes to premature aging and the development of neoplasms by affecting metabolism, extracellular matrix remodeling, inflammation, pigmentation, DNA repair, and apoptosis. This article provides an overview of the detrimental effects associated with sustained AHR activity in chronically stressed skin and pinpoints AHR as a promising target for chemoprevention.
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PMID:Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis. 3179 55