Life Extension Update
Tuesday, November 8, 2011. The October 15, 2011 issue of the journal Human Molecular Genetics published a report by researchers from Durham University in England and the University of Bologna in Italy concerning their discovery of a possible benefit for N-acetylcysteine in preventing and repairing DNA damage in Hutchinson-Gilford progeria syndrome (HGPS), one of several inherited diseases known as a laminopathies caused by mutations in the gene LMNA.
In their introductory remarks, Professor Christopher J. Hutchison and his associates note that "Fibroblasts from patients with the severe laminopathy diseases, restrictive dermopathy and Hutchinson Gilford progeria syndrome, are characterized by poor growth in culture, the presence of abnormally shaped nuclei and the accumulation of DNA double-strand breaks." (Fibroblasts are the most common type of cell in animal connective tissue, and are responsible for synthesizing collagen.) The team determined that the poor growth and double-strand breaks observed in the diseases are caused by high amounts of reactive oxygen species (a type of free radical that can react with and damage cells), as well as increased sensitivity to oxidative stress. While tests of normal fibroblasts showed efficient repair of double-strand breaks induced by reactive oxygen species, these breaks proved to be nonrepairable in fibroblasts from patients with laminopathy diseases. However, administration of N-acetylcysteine, a reactive oxygen species scavenger, resulted in a reduction in DNA double-strand breaks, elimination of unrepairable reactive-oxygen species-induced double-strand breaks, and improved growth.
"Our findings suggest that unrepaired reactive oxygen species-induced double-strand breaks contribute significantly to the restrictive dermopathy and HGPS phenotypes and that inclusion of NAC in a combinatorial therapy might prove beneficial to HGPS patients," the authors conclude.
"In children with progeria, we can see that double-strand breaks in the DNA architecture of cells increase which in turn adds to poor rates of cell growth," explained Dr Hutchison, who is a member of Durham University's Biophysical Sciences Institute. "Our treatment of these cells with the drug N-acetylcysteine (NAC) reversed both of these effects."
"Mutations in the LMNA gene cause more diseases, such as muscular dystrophy, than any other that we know," he observed. "We've found that DNA damage can be controlled and our findings could be an important step to helping both children with progeria and older people to live lives that are less debilitating in terms of health problems."
"We are using a careful approach that will look at patients with progeria to see if there's a model that can be used for wider medicine," Dr Hutchison added. "It would be great to find a way to help relieve some of the effects of progeria and to extend the children's lives, whilst also finding a way to help increasingly aging populations in many parts of the world. The findings are at a very early stage but they show the potential for helping people to live more comfortable and less painful lives when they reach 70 and 80 years of age and beyond."
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