title: Central administration of corticotropin-releasing factor induces tissue specific oxidative damage in chicks.
abstract: Corticotropin-releasing factor (CRF) modulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and has a key role in mediating neuroendocrine effects which occur in response to stressful stimuli. We have recently shown that intracerebroventricular (ICV) injection of CRF in neonatal chicks increased homeothermy that was associated with enhanced gene transcripts of mitochondrial fatty acid (FA) transport and oxidation enzymes in a tissue specific manner. These observations prompted an investigation into the potential role of CRF in a state of oxidative damage in different tissues. We therefore, investigated whether CRF-induced changes in metabolism are accompanied by oxidative damage in the plasma, brain and other tissues. Neonatal chicks (Gallus gallus) with or without ICV-CRF (42 pmol) were kept at thermoneutral temperature (30 degrees C). After 3 h, malondialdehyde (MDA) was measured in the plasma, brain, heart, liver and skeletal muscle (gastrocnemius). ICV-CRF significantly decreased the weight gain and feed consumption of chicks. Plasma, heart and liver revealed significantly higher MDA levels in chicks with ICV-CRF as compared to that of control chicks, but this pattern was not observed in the brain and muscle. Gene transcripts of enzymes involved in mitochondrial FA transport and oxidation, and 3-hydroxyacyl CoA dehydrogenase and citrate synthase enzyme activities in the brain were not changed by ICV-CRF. In conclusion, central administration of CRF in neonatal chicks induces tissue specific oxidative damage: higher MDA levels were observed in the heart and liver while no such change occurred in the brain and muscle.
authors.affiliation: Laboratory of Advanced Animal and Marine Bioresources, Faculty of Agriculture, Kyushu University, 6-10-1, Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan. ahmad@brs.kyushu-u.ac.jp
authors.forename: Ahmad
authors.initials: A
authors.lastname: Mujahid
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Furuse
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000235:genetics; D044942:Acyl-CoA Dehydrogenase, Long-Chain / Q000235:genetics; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002334:Carnitine O-Palmitoyltransferase / Q000235:genetics; D002645:Chickens / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D002950:Citrate (si)-Synthase / Q000235:genetics; D003346:Corticotropin-Releasing Hormone / Q000008:administration & dosage*; D005227:Fatty Acids / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D007276:Injections, Intraventricular; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D012333:RNA, Messenger; D008315:Malondialdehyde; D003346:Corticotropin-Releasing Hormone; D015094:3-Hydroxyacyl CoA Dehydrogenases; D044942:Acyl-CoA Dehydrogenase, Long-Chain; D002334:Carnitine O-Palmitoyltransferase; D002950:Citrate (si)-Synthase