Centrophenoxine Slows Down, but Does Not Reverse, Lipofuscin Accumulation in Cultured Cells

Summary: Centrophenoxine is not very interesting with regards to lipofuscin

Interestingness: 1

Paper by Alexei Terman and Martin Welander in the Journal of Anti-Aging Medicine, Volume 2, Issue 3, Fall 1999.

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Lipofuscin is made up of the residues from lysosome degradation. Wikipedia claims it is the product of oxidised unsaturated fatty acids. It doesn't degrade with time in the body by itself, it just accumulates. The age-spots in old people are made of this.

Centrophenoxine is a treatement for senile dementia, which wikipedia claims improves memory and general cognition.

They tried using centrophenoxine to stop formation of, and to get rid of lipofuscin in rat heart cells exposed to high levels of oxigen (to accelerate lipofuscin production is my guess, since they only left it for a few weeks). It reduced formation by about half at what seems to me to be very high concentrations (almost a millimole), but did didly for removing already established lipofuscin particles or modifying number of autophagic vacuoles induced by leupeptin. They attribute the reduction effect on its anti-oxidant properties
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Abstract follows:

Centrophenoxine, a drug used in the treatment of senile dementia, has been suggested to retard, or even reverse, lipofuscin accumulation within postmitotic cells. However, a true capacity of centrophenoxine to eliminate already formed lipofuscin inclusions has not been convincingly demonstrated. Moreover, no evidence has been obtained regarding the possible mechanisms through which intracellular content of lipofuscin would be diminished by centrophenoxine. Here we show that (a) centrophenoxine at concentrations of 0.25 or 0.5 mM diminishes lipofuscin accumulation within cultured neonatal rat cardiac myocytes (by 44% or 51%, respectively, during a period of 2 weeks) when it was constantly present in the culture medium; (b) the same treatment of rat cardiac myocytes and AG-1518 human f ibroblasts, however, does not eliminate already formed lipofuscin inclusions; (c) the formation of autophagic vacuoles, and ensuing degradation of their contents, are not influenced by centrophenoxine. Thus, our results do not support the idea that centrophenoxine can reverse age-related accumulation of lipofuscin. The observed decrease of lipofuscin formation is probably due to the previously shown antioxidant properties of centrophenoxine.