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Anchorage of Twisted Testis: A Rat Model of Ischemia-Reperfusion Injury of the Testis
Published on: November 14, 2025
Enhanced lipid peroxidation in tourniquet-release mice
Junko Adachi1, Emiko Kurisaki, Risa Kudo
1Department of Legal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. adachi@med.kobe-u.ac.jp <adachi@med.kobe-u.ac.jp>
Summary
Tourniquet-induced ischemia-reperfusion significantly increases oxidative stress markers, including 4-hydroxy-nonenal (HNE) in muscles and oxysterols in muscles, kidneys, and liver. This highlights the damaging effects of reperfusion injury on multiple organs.
Area of Science:
- Biomedical Science
- Physiology
- Pathology
Background:
- Ischemia-reperfusion injury involves reactive oxygen species and lipid peroxidation.
- Limited research exists on tourniquet-induced ischemia-reperfusion's impact on lipid peroxidation.
Purpose of the Study:
- To investigate if tourniquet-induced ischemia-reperfusion enhances lipid peroxidation.
- To quantify oxidative stress markers in muscles and organs following tourniquet release.
Main Methods:
- Tourniquet applied to mouse hind limb for 3 hours, followed by 5-60 minute reperfusion.
- Superoxide production assessed via 4-hydroxy-nonenal (HNE) immunohistochemistry.
- Oxysterols analyzed by HPLC in gastrocnemius muscles, kidneys, liver, heart, and lungs.
Main Results:
- Increased HNE immunoreactivity observed in reperfused gastrocnemius muscles, especially after 5 minutes.
- Elevated levels of various oxysterols detected in tourniquet-affected gastrocnemius muscles, kidneys, and liver.
- High blood urea nitrogen suggests kidney vulnerability to ischemia-reperfusion injury.
Conclusions:
- Ischemia-reperfusion following tourniquet release enhances oxidative stress.
- Increased HNE and oxysterols in muscles, kidneys, and liver indicate widespread peroxidation.
- Kidneys are particularly susceptible to damage from this type of injury.
