4.1 Article

Mitochondrial alterations in aging rat brain: effective role of (-)-epigallo catechin gallate

期刊

出版社

WILEY
DOI: 10.1016/j.ijdevneu.2009.01.003

关键词

Epigallo catechin gallate; Brain; Aging; Mitochondria; Oxidative stress

资金

  1. Indian Council of Medical Research, New Delhi
  2. Government of India
  3. Croatian Ministry of Science, Education and Sports
  4. COST Action B35

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Aging is a multi-factorial process which involves deprivation in body's metabolism. Brain mitochondria are prone to oxidative damage owing to their high metabolic rate. The decline in antioxidant system during aging augments the neuronal damage to mitochondrial components like antioxidant system, Kreb's cycle enzymes and electron transport chain complexes. Since brain is an organ rich in fatty acids, lipid peroxidation products like hydroxynonenal are predominant. Those lipid peroxidation products conjugate with amino acids to form adducts which alter their structural and functional properties. Epigallo catechin gallate is a potent antioxidant which is rich in green tea extract. This study elucidated the antioxidant potential of epigallo catechin gallate to counteract the mitochondrial oxidative damage in brain. The study comprised of young (3-4 months old; 150 + 20g) and aged (above 24 months; 420 +/- 20 g) male albino rats of Wistar strain in Groups I and II Groups III and IV comprised of young and aged rats supplemented with epigallo catechin gallate (2 mg/kg body weight) for 30 days. Antioxidants, Kreb's cycle enzymes and electron transport chain complexes were assayed in the mitochondrial fraction. Hydroxynonenal expression was carried out using immunohistochemical analysis. Epigallo catechin gallate supplementation decreased the expression of hydroxyrronenal in aged brain, up-regulated the antioxidant system and augmented the activities of Kreb's cycle enzymes and electron transport chain complexes in aged brain mitochondria thus proving its antioxidant potential at the level of mitochondria. (C) 2009 ISDN. Published by Elsevier Ltd. All rights reserved.

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