ArticleJournal of toxicology2026
Dexrazoxane Protects Against Hand-Foot Syndrome-Like Skin Damage in Pegylated Liposomal Doxorubicin-Treated Mice.
Article in Journal of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Dexrazoxane Protects Against Hand-Foot Syndrome-Like Skin Damage in Pegylated Liposomal Doxorubicin-Treated Mice.Journal of toxicology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anticancer drug pegylated liposomal doxorubicin (PLD) can cause hand-foot syndrome (HFS), a condition that develops in the palms and soles when pressure is frequently applied. Strategies to address HFS are insufficient. Dexrazoxane (DXZ) protects against doxorubicin-induced cardiotoxicity, possibly via reducing topoisomerase (Topo) IIβ levels in myocytes. Previously, we developed a rat model that used three tail-vein doses of PLD to induce HFS-like skin damage. In this study, we generated a simple mouse model of HFS-like skin damage using rubber fastening and PLD treatment to examine potential protective effects from DXZ. Male ddY mice received PLD (16.5 mg/kg) intravenously, with the flank skin compressed by a rubber band for 48 h. DXZ (50 and 250 mg/kg) was administered intraperitoneally twice prior to PLD. Skin tissues were removed on Day 12, fixed, and stained with hematoxylin-eosin to assess epidermal thickening. Western blotting identified the expression of γH2AX (a DNA damage marker) and the doxorubicin targets Topo IIα/β. After Day 8, DXZ (both concentrations) + PLD groups exhibited less skin damage than the PLD group. The PLD group showed greater epidermal layer thickening than both the control and DXZ + PLD groups. γH2AX and Topo IIβ expression increased in the back and flank regions of PLD-treated mice but was suppressed under DXZ + PLD treatment. Although not significant, Topo IIα expression followed an analogous pattern to Topo IIβ expression. In conclusion, we demonstrated that DXZ inhibited PLD-induced skin damage.
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Registered trials
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