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Chronic green tea or catechin treatment ameliorate rat hippocampal formation oxidative status
Author(s) -
Assunção Marco,
SantosMarques Maria João,
Carvalho Félix,
Andrade José Paulo
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a323-a
Subject(s) - glutathione , oxidative stress , lipid peroxidation , glutathione reductase , chemistry , catechin , superoxide dismutase , antioxidant , catalase , green tea extract , pro oxidant , ingestion , endocrinology , medicine , pharmacology , biochemistry , glutathione peroxidase , green tea , food science , enzyme , polyphenol
Evidence is accumulating that consumption of green tea (GT) may result in beneficial effects to brain redox status. As the hippocampal formation (HF) plays a pivotal role in cognitive functions and is especially prone to age‐related increase of pro‐oxidant factors, we intended to examine the effects of chronic GT or catechins ingestion on its redox status. Eighteen 12‐month old male Wistar rats were divided into three groups: control, GT and GT extract (GTE)‐treated animals. At 18 months of age, rats were sacrificed and the HF homogenized. Measurements of oxidative markers such as lipid peroxidation, protein carbonyls, glutathione, and antioxidant enzyme superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione S‐transferase (GST) activities were performed. Treatment with GT or GTE protected lipids and proteins against oxidative alterations compared to controls. Moreover, GT ingestion increased reduced glutathione and decreased oxidized glutathione levels relatively to control rats. GT‐ and GTE‐treated animals presented the highest SOD and CAT activities, respectively. In contrast, GR and GST activities were decreased in GT‐fed rats. Our results confirm the neuroprotective ability of GT catechins as shown by an improvement of HF oxidative status due probably to attenuation of age‐related oxidative stress. Granted by Unit 121/94 and SFRH/BD/19497/2004 from FCT.