منابع مشابه
Peroxisome senescence in human fibroblasts.
The molecular mechanisms of peroxisome biogenesis have begun to emerge; in contrast, relatively little is known about how the organelle functions as cells age. In this report, we characterize age-related changes in peroxisomes of human cells. We show that aging compromises peroxisomal targeting signal 1 (PTS1) protein import, affecting in particular the critical antioxidant enzyme catalase. The...
متن کاملBeryllium induces premature senescence in human fibroblasts.
After cells have completed a sufficient number of cell divisions, they exit the cell cycle and enter replicative senescence. Here, we report that beryllium causes proliferation arrest with premature expression of the principal markers of senescence. After young presenescent human fibroblasts were treated with 3 microM BeSO(4) for 24 h, p21 cyclin-dependent kinase inhibitor mRNA increased by >20...
متن کاملGlyoxal-induced premature senescence in human fibroblasts.
Mild stress-induced hormesis is an effective strategy to intervene in the aging process. Repeated exposure of human skin fibroblasts to 41 degrees C heat shock for 1 h twice a week is an example of mild stress that has many hormetic effects, including improved resistance to other stressors. We are now developing an experimental model system of sugar-induced premature senescence, which can be us...
متن کاملMagnesium deficiency accelerates cellular senescence in cultured human fibroblasts.
Magnesium inadequacy affects more than half of the U.S. population and is associated with increased risk for many age-related diseases, yet the underlying mechanisms are unknown. Altered cellular physiology has been demonstrated after acute exposure to severe magnesium deficiency, but few reports have addressed the consequences of long-term exposure to moderate magnesium deficiency in human cel...
متن کاملMild mitochondrial uncoupling prevents premature senescence in human dermal fibroblasts.
TO THE EDITOR Mitochondrial uncoupling, an increased permeability of the inner membrane to protons not coupled to ATP synthesis, dissipates mitochondrial membrane potential. Mild mitochondrial uncoupling is believed to prolong lifespan of certain model organisms by reducing the production of reactive oxygen species (ROS) and preventing oxidant damage (Brand, 2000). Indeed, long-lived Caenorhabd...
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ژورنال
عنوان ژورنال: Molecular Biology of the Cell
سال: 2002
ISSN: 1059-1524,1939-4586
DOI: 10.1091/mbc.e02-06-0322