Issue 29, 2024, Issue in Progress

Monitoring alterations of all-trans-retinal in human brain cancer cells by label-free confocal Raman imaging: regulation of the redox status of cytochrome c

Abstract

This article has shown the impact of all-trans-retinal on human brain cancer, which is apparent in the shifts in the redox status of cytochrome c in a single cell. The connection between cytochrome c expression and its role in cancer development remains relatively unexplored. To assess this, we employed Raman spectroscopy and imaging to determine the redox state of the iron ion in cytochrome c across different cellular locations, including mitochondria, cytoplasm, lipid droplets, and the endoplasmic reticulum within human brain cancer cells. We have analyzed normal human astrocytes (NHA) and two brain cancer cell lines (astrocytoma – CRL-1718 and glioblastoma – U-87 MG) without and supplemented with all-trans-retinal. Our results confirmed that human brain cancer cells demonstrate varying redox status compared to normal cells based on the established correlation between the intensity of the cytochrome c Raman band at 1583 cm−1 and the malignancy grade of brain cancer cells. Our research unveiled that all-trans-retinal induces remarkable changes in the mitochondrial functional activity (redox status) of cancer cells, which were measured by confocal Raman spectroscopy and imaging.

Graphical abstract: Monitoring alterations of all-trans-retinal in human brain cancer cells by label-free confocal Raman imaging: regulation of the redox status of cytochrome c

Supplementary files

Article information

Article type
Paper
Submitted
28 Feb 2024
Accepted
26 Jun 2024
First published
03 Jul 2024
This article is Open Access
Creative Commons BY-NC license

RSC Adv., 2024,14, 20982-20991

Monitoring alterations of all-trans-retinal in human brain cancer cells by label-free confocal Raman imaging: regulation of the redox status of cytochrome c

K. Jarczewska, M. Kopeć, H. Abramczyk and J. M. Surmacki, RSC Adv., 2024, 14, 20982 DOI: 10.1039/D4RA01542H

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