Abstract
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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
