Fruit flies provide an in vivo model to study ferroptosis and lifespan
Ferroptosis-inducing compounds shortened fly lifespan in a diet-dependent manner, while antioxidant treatment restored longevity and reversed iron-related changes in males.
Redox biology · Zhang L et al. · Paper published 28 Sep 2026
In fruit flies (Drosophila melanogaster), researchers examined how chemical triggers of ferroptosis alter survival, iron metabolism, and lipid biology. Exposure to the ferroptosis inducers erastin and RSL3 shortened fly lifespan in a dose- and diet-dependent manner. Co-treatment with the radical-trapping antioxidant ferrostatin-1 rescued lifespan in both sexes. In male w1118 flies, erastin increased the Fe2+/Fe3+ ratio and lowered ferritin-bound iron without altering total glutathione levels. RSL3 altered lipid composition in a manner consistent with lipid peroxidation. Although both sexes experienced shortened lifespans, these specific metabolic and lipid changes occurred only in males. Furthermore, complete knockout of the fly GPX4 ortholog Gtpx caused early lethality that was not rescued by ferrostatin-1.
Why it matters
Ferroptosis plays a key role in neurodegeneration and inflammatory diseases. Establishing an invertebrate model allows researchers to dissect how iron toxicity and lipid peroxidation influence aging and organismal survival.
Caveats
The biochemical markers of ferroptosis were detected only in male w1118 flies. In addition, fruit flies lack a clearly defined xCT ortholog and rely on a thioredoxin-dependent GPX4 counterpart rather than a selenocysteine enzyme.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
The fruitfly Drosophila melanogaster as an in vivo model of ferroptosis
Zhang L, Schmidt F, Yasar F et al.
Redox biology · 28 Sep 2026 · Peer-reviewed
- Relevance
- Relevant
- News value
- Notable
- Evidence
- Model organisms
- Status
- Peer-reviewed
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