Subcellular anti-atherosclerotic therapy: 5-aminolevulinic acid as a potential drug affecting dysfunctional mitochondria

Background and Aims: Earlier we found mithochondrial mutations associated with atherosclerosis. It is our assumption that elimination of mitochondria burdened with such mutations may be a novel approach to anti-atherosclerotic therapy. As a promising agent, we consider 5-aminolevulinic acid (5-ALA). Exogenous 5-ALA causes excessive accumulation of protoporfyrine IX (PpIX). PpIX is produced in mitochondria from 5-aminolevulinic acid (5-ALA) in course of heme synthesis cascade. In this work we studied 5-ALA-induced PpIX accumulation on mutation-bearing cybrid cell lines.