Hyperbaric oxygen augments Doxil antitumor efficacy by reducing tumor-induced lactate.
Level 5 - mechanism / opinion, no new human data
Preclinical laboratory and mechanistic research with no human data
PubMed 40889529 · doi:10.1016/j.jconrel.2025.114181
What was done
Researchers investigated how tumor-elevated lactate affects the hepatic clearance of the nanomedicine Doxil and whether hyperbaric oxygen intervention could mitigate this clearance mechanism to improve antitumor efficacy. The study evaluated the impact of hyperbaric oxygen on tissue glycolysis, lactate levels, Kupffer cell M2 polarization, hepatic Doxil uptake, circulation time, and antitumor response.
What was found
The abstract reports no quantitative values or statistical metrics. Qualitatively, tumor-derived lactate was reported to accelerate Doxil clearance by driving M2 polarization in Kupffer cells. Hyperbaric oxygen countered this by suppressing glycolysis and reducing lactate levels in tumors and normal tissues, which diminished M2 Kupffer cell polarization, reduced hepatic Doxil uptake, prolonged blood circulation time, and enhanced antitumor efficacy.
Why it matters
This work identifies a metabolic mechanism whereby tumor-derived lactate accelerates nanomedicine clearance and highlights hyperbaric oxygen as a potential strategy to improve liposomal drug delivery.
Limits
The abstract provides no sample sizes, numerical data, effect sizes, or specific model details. Findings are derived from preclinical mechanistic research with no human clinical validation.