Plasma Antioxidants and Human Aging: A Study on Healthy Elderly Tunisian Population

Chehab, Olfa; Ouertani, Mohamed Zied; Souiden, Yosra; Chaieb, Kamel; Mahdouani, Kacem

doi:10.1007/s12033-008-9056-5

Cited by 5 publications

(2 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is still an open question as to whether increased oxidative stress during aging is mainly caused by enhanced ROS production or decreased ROS scavenger activities, or both (Rao et al 1990; Liu & Mori 1993; Sohal et al 1994; Hussain et al 1995; Sandhu & Kaur 2002; Chehab et al 2008; Sasaki et al 2008). We found that although major ROS scavenger enzyme expression is increased in our Immp2l mutant mice, cellular oxidative stress is still elevated, supporting the notion that increased oxidative stress during aging is mainly caused by enhanced ROS production rather than decreased ROS scavenger activities (Sasaki et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…The role of these major antioxidant enzymes in aging is currently controversial. Some studies have reported a decrease in the expression or activities of these enzymes during aging (Rao et al, 1990;Sandhu & Kaur, 2002;Chehab et al, 2008). Others have found that expression levels were either unchanged or even slightly increased during aging (Liu & Mori, 1993;Sohal et al, 1994;Hussain et al, 1995;Sasaki et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial peptidase IMMP2L mutation causes early onset of age‐associated disorders and impairs adult stem cell self‐renewal

et al. 2011

View full text Add to dashboard Cite

SummaryMitochondrial reactive oxygen species (ROS) are proposed to play a central role in aging and ageassociated disorders, although direct in vivo evidence is lacking. We recently generated a mouse mutant with mutated Inner Mitochondrial Membrane Peptidase 2-like (Immp2l) gene, which impairs the signal peptide sequence processing of mitochondrial proteins cytochrome c1 and glycerol phosphate dehydrogenase 2. The mitochondria from mutant mice generate elevated levels of superoxide ion and cause impaired fertility in both sexes. Here we design experiments to examine the effects of excessive mitochondrial ROS generation on health span. We show that Immp2l mutation increases oxidative stress in multiple organs such as the brain and the kidney, although expression of superoxide dismutases in these tissues of the mutants is also increased. The mutants show multiple aging-associated phenotypes, including wasting, sarcopenia, loss of subcutaneous fat, kyphosis and ataxia, with female mutants showing earlier onset and more severe age-associated disorders than male mutants. The loss of body weight and fat was unrelated to food intake. Adipose derived stromal cells (ADSC) from mutant mice showed impaired proliferation capability, formed significantly less and smaller colonies in colony formation assays, although they retained adipogenic differentiation capability in vitro. This functional impairment was accompanied by increased levels of oxidative stress. Our data showed that mitochondrial ROS is the driving force of accelerated aging and suggested that ROS damage to adult stem cells could be one of the mechanisms for age-associated disorders.

show abstract