Researchers at RIKEN Turn Cancer’s Carbon Monoxide Into a Treatment Drug
A metal catalyst enclosed in an albumin protein carrier can travel through the bloodstream and use excess carbon monoxide produced by malignant cells to manufacture phenanthridinone anticancer drugs directly inside the tumor. Katsunori Tanaka led the research team at the RIKEN Pioneering Research Institute in Japan, publishing the findings in Nature Communications. Traditional chemotherapy attacks both malignant and healthy tissue indiscriminately, creating severe side effects for patients. This experimental approach seeks to deploy relatively harmless compounds that activate only upon entering cancer cells.
Palladacycles and Albumin Protein Protection Against Cellular Deactivation
The core mechanism relies on palladacycles, which are metal-containing compounds that react with carbon monoxide to produce phenanthridinone, an organic molecule integrated into existing anticancer medications. Without protection, substances like glutathione inside living cells rapidly deactivate the central palladium catalyst and halt the reaction. To solve this obstacle, Tanaka’s laboratory enclosed the palladacycle within albumin, a common blood protein. This carrier shields the palladium complex as it travels through the body, allowing it to reach target tissues without premature deactivating reactions.
Laboratory Tests on Human Liver, Cervical, Breast, and Lung Cancer Cells
The research team evaluated the drug-generating system by exposing cultured human liver, cervical, breast, and lung cancer cell lines to the albumin-palladacycle complex for 48 hours. They simultaneously tested a noncancerous cell line to verify whether the reaction would trigger in healthy tissue. Phenanthridinone appeared in all the cancer cell lines after the 48-hour period but was entirely absent in normal cells. Further system modifications enabled the newly formed compound to detach from the carrier and move freely, generating a highly toxic derivative that damaged the cultured liver cancer cells from the inside out.
Hemoglobin Binding Prevents Premature Toxic Drug Formation in Blood
An immediate safety concern involved the carbon monoxide already circulating through the human bloodstream, which could theoretically trigger the chemical reaction prematurely and damage healthy blood cells. Laboratory testing confirmed that the toxic drug did not form in blood samples. Researchers attribute this safety barrier to the fact that carbon monoxide in the bloodstream largely binds to hemoglobin, the protein responsible for oxygen transport, rendering the gas unavailable for the catalytic reaction. This indicates the delivery system can travel through the circulatory system safely, though in vivo testing remains necessary.
Frequently Asked Questions About the Cancer-Fighting Carbon Monoxide Method
How does the albumin carrier protect the palladium catalyst inside the body?
The albumin protein encloses the palladacycle, shielding the palladium catalyst from cellular substances like glutathione that would otherwise deactivate it before it reaches the tumor.
Why doesn’t the chemical reaction trigger inside the human bloodstream?
Carbon monoxide in the blood binds primarily to hemoglobin for oxygen transport, making it unavailable to react with the palladium catalyst until it encounters tumors.
What type of anticancer compound does this chemical reaction produce?
The reaction produces phenanthridinone and specific toxic derivatives that are already utilized in established anticancer drugs.
Where was this research conducted and published?
The study was led by Katsunori Tanaka at the RIKEN Pioneering Research Institute in Japan and published in Nature Communications.