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Intermittent hypoxia and isoniazid plus rifampicin affect hepatic ultrastructure in mice
Run-Hua Wu1, Yi-Ming Zeng, Xiao-Yang Chen
1Department of Pulmonary Medicine, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Background:
Chronic intermittent hypoxia is the most important pathophysiologic feature of sleep apnea syndrome. The present study aimed to determine whether chronic intermittent hypoxia, which is associated with sleep apnea syndrome, can cause or increase damage to liver cell ultrastructure induced by isoniazid and rifampicin in mice.
Methods:
Based on a 2 × 2 full factorial design consisting of two factors of chronic intermittent hypoxia and isoniazid plus rifampicin, 32 male C57B6J mice were randomized into the control group, the chronic intermittent hypoxia group, the isoniazid plus rifampicin group, and the chronic intermittent hypoxia + isoniazid plus rifampicin group. Twelve weeks after treatment, we examined the ultrastructure of liver cells and quantitatively analyzed mitochondrial morphology in C57B6J mice.
Results:
Chronic intermittent hypoxia did not significantly affect the ultrastructure of liver cells. The main effect of chronic intermittent hypoxia did not lead to an increase of mean profile area or mean perimeter of mitochondria, and a decrease of numerical density on area of mitochondria (all P > 0.05). Isoniazid plus rifampicin significantly affected liver cell ultrastructure. The main effect of isoniazid plus rifampicin resulted in an increase of mean profile area and mean perimeter of mitochondria, and a decrease of numerical density on area of mitochondria (all P < 0.05). Moreover, there was a positive interaction among the chronic intermittent hypoxia and the isoniazid plus rifampicin groups for mean profile area, mean perimeter, and numerical density on area of mitochondria (all P < 0.05).
Conclusion:
Chronic intermittent hypoxia and isoniazid plus rifampicin treatment lead to synergistic liver cell ultrastructural injury.
Insights
Chronic intermittent hypoxia and tuberculosis drug treatment synergistically damage liver cells. This study investigated how these factors interact to affect liver cell ultrastructure and mitochondrial morphology in mice.
Area of Science:
- Hepatology
- Toxicology
- Sleep Medicine
Background:
- Sleep apnea syndrome is characterized by chronic intermittent hypoxia.
- This study investigates the impact of chronic intermittent hypoxia on liver cell damage induced by isoniazid and rifampicin.
Purpose of the Study:
- To determine if chronic intermittent hypoxia exacerbates liver cell ultrastructural damage caused by isoniazid and rifampicin in mice.
Main Methods:
- A 2x2 factorial design involved 32 mice exposed to chronic intermittent hypoxia and/or isoniazid plus rifampicin for 12 weeks.
- Liver cell ultrastructure and mitochondrial morphology were quantitatively analyzed.
Main Results:
- Isoniazid plus rifampicin significantly altered liver cell ultrastructure, increasing mitochondrial size and decreasing mitochondrial density.
- Chronic intermittent hypoxia alone did not significantly affect liver cell ultrastructure.
- A synergistic interaction was observed between chronic intermittent hypoxia and drug treatment, worsening liver cell injury.
Conclusions:
- Combined exposure to chronic intermittent hypoxia and isoniazid plus rifampicin results in synergistic liver cell ultrastructural injury.
- This highlights a significant interaction between sleep apnea-related hypoxia and tuberculosis treatment toxicity.
