TY - JOUR
T1 - Central administration of corticotropin-releasing factor induces tissue specific oxidative damage in chicks
AU - Mujahid, Ahmad
AU - Furuse, Mitsuhiro
N1 - Funding Information:
This work was supported by a Grant-in-Aid for Japan Society for the Promotion of Science (JSPS) Postdoctoral Fellowship for Foreign Researchers to M.A. (No.197179) and a Grant-in-Aid for Scientific Research from JSPS to M.F. (No. 18208023).
PY - 2008/12
Y1 - 2008/12
N2 - 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 °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.
AB - 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 °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.
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U2 - 10.1016/j.cbpa.2008.08.013
DO - 10.1016/j.cbpa.2008.08.013
M3 - Article
C2 - 18786646
AN - SCOPUS:54349124025
VL - 151
SP - 664
EP - 669
JO - Comparative biochemistry and physiology. Part A, Molecular & integrative physiology
JF - Comparative biochemistry and physiology. Part A, Molecular & integrative physiology
SN - 1095-6433
IS - 4
ER -