Real-time monitoring of spatial and temporal metabolic changes during focal cerebral ischemia in rats

Livnat, Amir; Barbiro-Michaely, Efrat; Mayevsky, Avraham

doi:10.1016/j.brainres.2011.03.008

Cited by 4 publications

(1 citation statement)

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“…In rats, focal ischemia or ischemia/reperfusion has led to a decrease in ADP-stimulated and uncoupled respiration rates, with a marked fall in the respiratory control ratio [70], a transient decrease in complex IV activity [71] or a robust decline in complex IV activity [72], release of mitochondrial cytochrome c [73], potential activation of the mitochondrial permeability transition pore [74], a reduction in mitochondrial DNA content [75], depletion of mitochondrial glutathione [76], and a reversal of ATP synthetase activity [77]. Differences in mitochondrial function in the core and penumbral region of ischemia have also been reported [78]. It should however be noted that administration of 3-nitropropionic acid (3-NP), a miochondrial toxin, to rats prior to ischemia in order to induce tolerance, has resulted in decreased cerebral damage [79].…”

Section: Oxidative Stress and Mitochondrial Dysfunction In Neuronamentioning

confidence: 99%

Effect of Polyphenols on Oxidative Stress and Mitochondrial Dysfunction in Neuronal Death and Brain Edema in Cerebral Ischemia

Panickar

Anderson

2011

IJMS

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Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti-inflammatory, anti-carcinogenic, anti-viral, anti-ulcer, and anti-apoptotic properties. One important consequence of ischemia is neuronal death and oxidative stress plays a key role in neuronal viability. In addition, neuronal death may be initiated by the activation of mitochondria-associated cell death pathways. Another consequence of ischemia that is possibly mediated by oxidative stress and mitochondrial dysfunction is glial swelling, a component of cytotoxic brain edema. The purpose of this article is to review the current literature on the contribution of oxidative stress and mitochondrial dysfunction to neuronal death, cell swelling, and brain edema in ischemia. A review of currently known mechanisms underlying neuronal death and edema/cell swelling will be undertaken and the potential of dietary polyphenols to reduce such neural damage will be critically reviewed.

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