A Ginkgo Biloba Extract (EGb 761) Prevents Mitochondrial Aging by Protecting Against Oxidative Stress

Sastre, Juan; Millán, A; Asunción, José García de la; Plá, Rosa Corcoy i; Juan, Gloria; Pallardó, Federico V.; O’Connor, Enrique; Martín, J.A.; Droy-Lefaix, Marie-Thérèse; Viña, José

doi:10.1016/s0891-5849(97)00228-1

Cited by 195 publications

(144 citation statements)

References 36 publications

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“…24 Disorders of mtDNA produce abnormalities in mitochondrial morphology and function. 25,26 Our present Table 5 Quantitative real-time PCR data for antioxidants in rat kidney…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that prevention of oxidative stress by antioxidant treatment also prevents age-related decreases in mitochondrial membrane potential and increases in mitochondrial size. 25 Therefore, antioxidant therapy might be useful for the preservation of mitochondrial function. Mitochondrial damage can occur as a consequence of the disease processes.…”

Section: Discussionmentioning

confidence: 99%

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Mitochondrial damage-induced impairment of angiogenesis in the aging rat kidney

Satoh

Fujimoto

Horike

et al. 2011

Laboratory Investigation

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Decreased expression of vascular endothelial growth factor (VEGF) in the renal tubules is thought to cause progressive loss of the renal microvasculature with age. Mitochondrial dysfunction may be a principal phenomenon underlying the process of aging. The relation between VEGF expression and mitochondrial dysfunction in aging is not fully understood. We hypothesized that mitochondrial dysfunction blocks VEGF expression and contributes to impaired angiogenesis in the aging kidney. The aim of this study was to assess the role of mitochondria in VEGF expression in the aging rat kidney. We evaluated the accumulation of 8-hydroxy-2 0 -deoxyguanosine in mitochondrial DNA, as well as mitochondrial dysfunction, as assessed by electron microscopy of mitochondrial structure and histochemical staining for respiratory chain complex IV, in aging rat kidney. An increase in hypoxic area and a decrease in peritubular capillaries were detected in the cortex of aging rat kidneys; however, upregulation of VEGF expression was not observed. The expression of VEGF in proximal tubular epithelial cells in response to hypoxia was suppressed by the mitochondrial electron transfer inhibitor myxothiazol. Mitochondrial DNA-deficient cells also failed to upregulate VEGF expression under hypoxic conditions. These results indicate that impairment of VEGF upregulation, possibly as a result of mitochondrial dysfunction, contributes to impaired angiogenesis, which in turn leads to renal injury in the aging rat kidney.

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“…24 Disorders of mtDNA produce abnormalities in mitochondrial morphology and function. 25,26 Our present Table 5 Quantitative real-time PCR data for antioxidants in rat kidney…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mitochondrial damage-induced impairment of angiogenesis in the aging rat kidney

Satoh

Fujimoto

Horike

et al. 2011

Laboratory Investigation

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“…In aged rats and humans, however, there are a smaller number of larger mitochondria; however, the total volume of mitochondria (up to 20% of cell volume) remains roughly the same in young and old rats/humans. These larger, mega-mitochondria are not as bio-energetically efficient as the small mitochondria (Sastre et al 1998;Wakabayashi 2002). …”

Section: Mitochondrial Statusmentioning

confidence: 98%

Normal brain ageing: models and mechanisms

Toescu

2005

Phil. Trans. R. Soc. B

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Normal ageing is associated with a degree of decline in a number of cognitive functions. Apart from the issues raised by the current attempts to expand the lifespan, understanding the mechanisms and the detailed metabolic interactions involved in the process of normal neuronal ageing continues to be a challenge. One model, supported by a significant amount of experimental evidence, views the cellular ageing as a metabolic state characterized by an altered function of the metabolic triad: mitochondria-reactive oxygen species (ROS)-intracellular Ca 2C . The perturbation in the relationship between the members of this metabolic triad generate a state of decreased homeostatic reserve, in which the aged neurons could maintain adequate function during normal activity, as demonstrated by the fact that normal ageing is not associated with widespread neuronal loss, but become increasingly vulnerable to the effects of excessive metabolic loads, usually associated with trauma, ischaemia or neurodegenerative processes. This review will concentrate on some of the evidence showing altered mitochondrial function with ageing and also discuss some of the functional consequences that would result from such events, such as alterations in mitochondrial Ca 2C homeostasis, ATP production and generation of ROS.

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“…10) Recent studies of mitochondria from brain, liver or heart cells exposed to hypoxia and/or ischemic stress show the protective effect of Gb extract against oxidative stress and also a limiting effect membrane lipoperoxidation. [11][12][13][14][15] In our investigation, we aimed to determine the effect of prolonged Gb extract treatment on free radical production by phagocytic cells. Results clearly confirmed that hypoxia exposure induced an overproduction of free oxygen radicals and that Gb extract treatment induced a decrease in CL intensity compared to control rats for both dilutions and stimuli.…”

Section: Resultsmentioning

confidence: 99%