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Mitochondrial modulation of apoptosis induced by low-dose radiation in mouse testicular cells
Fang Fang1, Ping Sheng Gong, Hong Guang Zhao
1Key Laboratory of Radiobiology, Ministry of Health, School of Public Health, Jilin University, Changchun 130021, Jilin, China.
Objective:
To investigate whether apoptosis induced by low-dose radiation (LDR) is regulated by mitochondrial pathways in testicular cells.
Methods:
Male mice were exposed to whole-body LDR, and changes in mitochondrial function and in expression of apoptotic factors were analyzed in the testicular cells as follows. Total nitric-oxide synthase (T-NOS) and Na+/K+ ATPase activities were biochemically assayed. Reactive oxygen species (ROS) and mitochondrial membrane potential (Δψm) were determined by flow cytometry using fluorescent probes. Levels of mRNAs encoding cytochrome c (Cyt c) and apoptosis-inducing factor (AIF) were quantified by real-time reverse-transcription PCR (RT-PCR). Expression of Cyt c, AIF, caspase-9, and caspase-3 at the protein level was assessed by western blotting and immunohistochemistry.
Results:
LDR induced an increase in T-NOS activity and ROS levels, and a decrease in Na+/K+ ATPase activity and mitochondrial Δψm, in the testicular cells. The intensity of these effects increased with time after irradiation and with dose. The cells showed remarkable swelling and vacuolization of mitochondria, and displayed a time- and dose-dependent increase in the expression of Cyt c, AIF, procaspase-9, and procaspase-3. Activation of the two procaspases was confirmed by detection of the cleaved caspases. The changes in expression of the four apoptotic factors were mostly limited to spermatogonia and spermatocytes.
Conclusion:
LDR can induce testicular cell apoptosis through mitochondrial signaling pathways.
Insights
Low-dose radiation (LDR) triggers testicular cell apoptosis via mitochondrial pathways. This study reveals LDR impacts mitochondrial function and apoptotic factor expression in male mice testes.
Area of Science:
- Cell Biology
- Radiation Biology
- Mitochondrial Biology
Background:
- Low-dose radiation (LDR) effects on reproductive health are not fully understood.
- Mitochondrial pathways play a critical role in cellular apoptosis.
Purpose of the Study:
- To investigate the role of mitochondrial pathways in LDR-induced apoptosis in testicular cells.
- To analyze changes in mitochondrial function and apoptotic factor expression following LDR exposure.
Main Methods:
- Male mice exposed to whole-body LDR.
- Assessed nitric-oxide synthase (T-NOS) and Na+/K+ ATPase activities.
- Measured reactive oxygen species (ROS) and mitochondrial membrane potential (Δψm) via flow cytometry.
- Quantified mRNA and protein levels of cytochrome c (Cyt c), apoptosis-inducing factor (AIF), caspase-9, and caspase-3.
Main Results:
- LDR increased T-NOS activity and ROS, decreased Na+/K+ ATPase activity and Δψm.
- Mitochondrial swelling and vacuolization observed.
- Time- and dose-dependent increases in Cyt c, AIF, procaspase-9, and procaspase-3 expression and activation.
- Changes primarily affected spermatogonia and spermatocytes.
Conclusions:
- LDR induces testicular cell apoptosis.
- Mitochondrial signaling pathways are key regulators of LDR-induced testicular apoptosis.
