Korean J Psychopharmacol.
2000 Sep;11(3):238-246.
Changes of Antioxidant Enzyme Activities of Rat Brain in the Stress-Related Responses
- Affiliations
-
- 1Department of Psychiatry, College of Medicine, Yeungnam University, Taegu, Korea. jblee@medical.yeungnam.ac.kr
- 2Department of Pharmacology, College of Medicine, Yeungnam University, Taegu, Korea.
- 3Kwangjang Neuropsychiatric Clinic, Taegu, Korea.
- 4Department of Psychiatry, Catholic University of Taegu School of Medicine, Taegu, Korea.
Abstract
- Renin-Angiotensin system (RAS) has been suggested as one of important factors in stress-related responses, and also suggested to be a pro-oxidant in mammals. Studies about antioxidant activity changes in brain by systemic administration of angiotensin II (Ang II) may be valuable data in the clarification of pathogenesis and development of treatment modalities for the psychologic stress-induced somatic disease, such as stress-induced hypertension. We examined, therefore, antioxidant defense changes in the brain induced by Ang II. Antioxidant enzyme activities including superoxide dismutase (SOD), contents of glutathione (GSH), and lipoperoxidation (LPO) were measured in the dissected specimens of the brain regions after subcutaneous injection of human Ang II. In this study, peripheral administration of Ang II decreased LPO in the cerebral cortex, hippocampus, striatum, hypothalamus of Sprague-Dawley rats. Ang II increased activities of SOD, glutathione peroxidase, and glutathione reductase in the hippocampus and striatum. Borderline-hypertensive rats (BHR), a well-known animal model for stress-induced hypertension, showed some differences in the Ang II-induced antioxidant activity changes, comparing with SD rats. In the BHR, peripheral administration of Ang II significantly decreased the activities of antioxidant enzymes and contents of GSH, increased LPO contents in the various regions of brain. These results suggested that oxidative stress on the brain due to Ang II may be greater in the BHR than SDs, and RAS may be one of important pathophysiologic factors for stress-induced hypertension in BHR.
MeSH Terms
-
Angiotensin II
Animals
Brain*
Cerebral Cortex
Glutathione
Glutathione Peroxidase
Glutathione Reductase
Hippocampus
Humans
Hypertension
Hypothalamus
Injections, Subcutaneous
Mammals
Models, Animal
Oxidative Stress
Rats*
Rats, Sprague-Dawley
Renin-Angiotensin System
Superoxide Dismutase
Angiotensin II
Glutathione
Glutathione Peroxidase
Glutathione Reductase
Superoxide Dismutase
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