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Related Experiment Video

Updated: Jan 6, 2026

A Photodynamic Approach to Study Function of Intracellular Vesicle Rupture

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Programmed Cell Death via Type IV Photodynamic Therapy Using Internalized Two-Photon Activated Molecular

Thomas S Bradford¹, Dongdong Liu², James M Tour³

¹Department of Chemistry, Durham University, South Road, Durham DH1 3LE, United Kingdom.

ACS Applied Bio Materials

|October 13, 2025

Summary

Direct photodynamic therapy (PDT) uses molecular nanomachines (MNMs) to eliminate cancer cells. This novel approach avoids reactive oxygen species (ROS) and offers tunable cell death mechanisms for safer cancer treatment.

Keywords:

2PE MNM NIR activation PDT multiphoton nanomachines

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Photodynamic Therapy with Blended Conducting Polymer/Fullerene Nanoparticle Photosensitizers

Photodynamic Therapy with Blended Conducting Polymer/Fullerene Nanoparticle Photosensitizers

Published on: October 28, 2015

Area of Science:

Biomedical Engineering
Nanotechnology
Cancer Therapy

Background:

Direct photodynamic therapy (PDT) is an emerging cancer treatment alternative.
Unlike indirect PDT, direct PDT utilizes photosensitizers (PS) to directly damage cancer cells, avoiding reactive oxygen species (ROS).
Previous research introduced near-infrared light-activated molecular nanomachines (MNMs) for cell-specific necrosis via membrane disruption.

Purpose of the Study:

To extend prior work on MNMs for cancer treatment.
To investigate modifications of MNMs for enhanced cellular uptake and targeted mitochondrial localization.
To demonstrate a novel mechanism of programmed cell death (PCD) induction by light-activated MNMs.

Main Methods:

Modified MNMs with polyethylene glycol (PEG) or triphenol phosphonium (TPP+) functional groups were synthesized.
Cellular uptake and mitochondrial localization of modified MNMs were assessed.
Light-induced activation of MNMs was performed to evaluate cell death mechanisms (necrosis vs. PCD).

Main Results:

PEG and TPP+ modifications enabled MNMs to cross the phospholipid bilayer and localize at the mitochondrial membrane.
MNM activation induced programmed cell death (PCD) without compromising cellular membrane integrity.
The same MNM technology could induce either necrotic or PCD cell death by altering the excitation procedure.

Conclusions:

Modified MNMs offer a promising platform for targeted cancer therapy.
This technology enables tunable induction of cell death, offering a cleaner therapeutic approach.
Light-activated MNMs represent a significant advancement in cancer treatment, providing versatile cell elimination strategies.