Mitochondria, oxidative stress and aging

Abstract

In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDNA), are major targets of free radical attack. At present, it is well established that mitochondrial deficits accumulate upon aging due to oxidative damage. Thus, oxidative lesions to mtDNA accumulate with age in human and rodent tissues. Furthermore, levels of oxidative damage to mtDNA are several times higher than those of nuclear DNA. Mitochondrial size increases whereas mitochondrial membrane potential decreases with age in brain and liver. Recently, we have shown that treatment with certain antioxidants, such as sulphur-containing antioxidants, vitamins C and E or the Ginkgo biloba extract EGb 761, protects against the age-associated oxidative damage to mtDNA and oxidation of mitochondrial glutathione. Moreover, the extract EGb 761 also prevents changes in mitochondrial morphology and function associated with aging of the brain and liver. Thus, mitochondrial aging may be prevented by antioxidants. Furthermore, late onset administration of certain antioxidants is also able to prevent the impairment in physiological performance, particularly motor co-ordination, that occurs upon aging.

Experimental Study on the Neuronal Toxical Effect of Levodopa and the Inhibition of Ginkgo Biloba Extract on Parkinson Disease in Rats

“…EGb and ginkgo lactone can inhibit dopaminergic metabolism of striatum and limbic system [10]. EGb prevents not only injury of mitochondria DNA, but also mitochondria function and morphologic change [11]. In our study, we found that number of apoptosis in E-D group was lower 33.4%, 40.8%, 35.7% than L-dopa group in 10d, 12d, 14d.…”

Genetic Ablation of Calcium-independent Phospholipase A2γ Leads to Alterations in Hippocampal Cardiolipin Content and Molecular Species Distribution, Mitochondrial Degeneration, Autophagy, and Cognitive Dysfunction

“…Aging is associated with a decreased capacity to generate ATP by oxidative phosphorylation due primarily to diminished complex I and IV activity in mitochondria (6,64,66). Increases in mitochondrial size and decreased membrane potential are present during aging and likely lead to mitochondrial dysfunction through oxidative damage (67). The enlarged mitochondria observed during aging often contain concentric multilamellar structures that were observed in a neuronal cell line highly susceptible to oxidative stress (63) as well as in patients with Barth syndrome.…”

Protective effects of probioticLactobacillus plantarumBJ0021 on liver and kidney oxidative stress and apoptosis induced by endosulfan in pregnant rats

“…Malondialdehyde (MDA) was measured according to the method described by Sastre et al 35 Liver and kidney homogenates 10% (w/v) were prepared in 0.1 Mol/L TrisHCl buffer, pH 7.4. An aliquot of the homogenate is then precipitated with 10% trichloroacetic acid (w/v) and added with thiobarbituric acid 0.67% (w/v).…”