Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Jan 25;11:673–681. doi: 10.1016/j.redox.2017.01.017

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2017 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Fig. 5. — Effects of reduced mitophagy on lipofuscin formation during SIPS. To investigate the influence of mitophagy inhibition on lipofuscin formation, young fibroblasts were co-treated with the mitochondrial division inhibitor 1 (Mdivi-1) during PQ-induced SIPS. Panel A shows the accumulation of lipofuscin after SIPS with or without inhibition of mitochondrial division. Lipofuscin-specific autofluorescence intensity was measured at Cell Lab Quanta™ SC MPL flow cytometer (Beckman Coulter, Krefeld, Germany) after excitation with a UV lamp (360 nm) and an emission of 525 nm. Panel B illustrates changes of the mitochondrial mass during SIPS. Mitochondrial superoxide radical formation was estimated using MitoSOX (C). In Panel D, the amounts of protein carbonyls are shown. Protein carbonyls were determined by Oxyblot. The formation of free radicals was determined by DCF fluorescence measurement (E). Panel F shows the cellular viability after SIPS treatment, assessed by propidium iodide staining. Statistically significant differences to the control are indicated by ‘*’, compared to respective SIPS by a ‘#’.