Regional lipid peroxidation in rat brain in vitro: Possible role of endogenous iron

Zaleska, Małgorzata; Floyd, Robert A.

doi:10.1007/bf00964608

Cited by 228 publications

(82 citation statements)

References 22 publications

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“…In the 8-mo-olds, significant increases (P < 0.05) were seen in the CC of all the groups and this was with respect to the unsupplemented sedentary. Among the middle-aged, exercise training and Vitamin E significantly increased the SOD in both the regions (HC, 35.6% in SW-T, E; CC, 33.8%, SW-T, E of SE-C, N) (P < 0.05). Sedentary when supplemented with Vitamin E showed significant increase in enzyme activity in the HC (23.0% of SE-C, N) (P < 0.05) and CC (33.0% of SE-C, N).…”

Section: Tissue Antioxidantsmentioning

confidence: 93%

Regional responses in antioxidant system to exercise training and dietary Vitamin E in aging rat brain

Devi

Kiran

2004

Neurobiology of Aging

130

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We have evaluated the effect of exercise, Vitamin E and a combination of both on the antioxidant enzymes (AOEs)-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) along with the products of lipid peroxidation (LP)-malondialdehyde (MDA) and lipofuscin-like auto fluorescent substances (LF-like AFS) in discrete brain regions of rats of 4 (young adults), 8 (old adults), 12 (middle-age) and 22 months (mos) old of age. Hippocampus (HC) showed greater increase in GSH-Px activity than cerebral cortex (CC) to exercise and Vitamin E and was irrespective of the age. A combination of both was effective in the CC of all age groups but not in the supplemented sedentary of 12-and 22-mo-olds. CAT activity increased significantly in the HC of supplemented and trained rats but not in the combination group of any age. SOD increased in both the regions of supplemented trainees. However, old were more benefited in terms of maximal elevation in the HC. Vitamin E reduced MDA content in both regions of adult. LF-like AFS decreased significantly in supplemented sedentary and trainees of all ages. Our results demonstrate that an age-related deficit in AOEs in the CC and HC can be overcome through Vitamin E plus exercise, and further suggests the rationale for looking at these markers of oxidative stress in several age-related neuronal diseases.

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Section: Tissue Antioxidantsmentioning

confidence: 93%

Regional responses in antioxidant system to exercise training and dietary Vitamin E in aging rat brain

Devi

Kiran

2004

Neurobiology of Aging

130

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“…Fe 2+ is released from surrounding cells and iron-binding proteins during transient focal ischemia. The released Fe 2+ can also convert hydrogen peroxide to hydroxyl radical, and may mediate lipid peroxidation during reperfusion (White et al, 1985;Zaleska and Floyd, 1985). Late-onset iron deposition was also observed after transient focal ischemia in rat brain (Kondo et al, 1995).…”

Section: Production Of Reactive Oxygen Species By Transition Metalsmentioning

confidence: 99%

Cellular and Molecular Pathways of Ischemic Neuronal Death

Won¹,

Kim²,

Gwag³

2002

BMB Reports

201

172

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Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca 2+ and Na + that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

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“…Iron is abundant in the CNS and is in part responsible for the increased susceptibility of the brain to oxidative damage, particularly LP 27 . Because it is a strong inducer of LP, the levels of low molecular weight forms of redox-active iron are tightly regulated and maintained at extremely low levels under physiological conditions.…”

Section: Discussionmentioning

confidence: 99%