Rat and cell study: TBP exposure linked to liver aging via fumarate and mtDNA escape
In rats and BRL-3A cells, tributyl phosphate exposure was associated with markers of liver aging; the abstract proposes fumarate-driven mitochondrial DNA escape and FPR2 activation as the pathway. [1]
Automatic summary · not editorially reviewed
The key findings
Rats and BRL-3A cells were treated with tributyl phosphate, a possible environmental trigger of liver aging. [1]
TBP was reported to cause cell cycle arrest and raise β-galactosidase, ROS and MMP-1 levels. [1]
The abstract proposes that TBP-raised fumarate drives mtDNA escape and FPR2 activation, triggering liver aging in rats. [1]
The source at a glance
- Study type / format
- Laboratory study in rats and a cell line (abstract)
- Population / context
- Rats and BRL-3A cells treated with tributyl phosphate
- Summary based on
- Study abstract
- Original publication
- October 9, 2026
TBP exposure in rats and BRL-3A cells
The abstract describes a laboratory study in which rats and BRL-3A cells were treated with tributyl phosphate (TBP), identified as a possible environmental trigger of liver aging. Liver aging here is described as distinct from chronological aging and mainly driven by environmental factors. The authors asked how TBP might act. This is an abstract; the full text was not reviewed.
Supporting source [1]
Senescence markers and proposed fumarate–mtDNA–FPR2 route
TBP was reported to cause cell cycle arrest, higher β-galactosidase activity, and elevated ROS and MMP-1 levels, with increased p53, lys9 and γ-H2A.X protein expression, while HP1 protein was inhibited in rat livers and cells. The abstract concludes that TBP raises fumarate levels, which directly drives mitochondrial DNA (mtDNA) escape and activates FPR2, finally triggering liver aging in rats. These are associations and a proposed mechanism, not proof of cause in humans.
Supporting source [1]
Intervention tools and limits of this abstract
To probe the pathway, the researchers used WRW4, ethidium bromide, Lv-FH and monomethyl fumarate to model FPR2 inhibition, depletion of cytoplasmic mtDNA, fumarate clearance and fumarate supplementation. The abstract does not report sample sizes, doses, follow-up duration or effect sizes, and the full text was not reviewed. Findings come from rats and a cell line, so they do not establish human lifespan or health benefits.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Sample sizes, doses, follow-up and effect sizes are not reported. Results are from rats and BRL-3A cells and do not establish human outcomes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Yang L, Qian H, Ge Z, Wang T, Zhang J, Shi J, Jiang H, Zhang X, Lv Y, Zhou L. · europepmc.org · October 9, 2026