Cisplatin-Induced Testicular Toxicity and Protective Mechanisms
Summary
Cisplatin, a cornerstone of chemotherapeutic regimens against a variety of solid tumours, exerts dose‐limiting toxicity on the male reproductive system. Testicular damage arises through the generation of excessive reactive oxygen species, leading to oxidative stress, lipid peroxidation, DNA strand breaks and activation of intrinsic apoptotic pathways. Germ cell depletion, disruption of Sertoli–germ cell junctions and impairment of Leydig cell steroidogenesis culminate in diminished sperm count, motility and testosterone synthesis. Contemporary research seeks to mitigate these effects by targeting antioxidant defence systems, modulating inflammatory and apoptotic signalling cascades, and harnessing regenerative approaches such as mesenchymal stem cell therapy. Elucidation of molecular underpinnings, including the role of autophagy, the Nrf2 pathway and mitochondrial integrity, has paved the way for adjunctive interventions that may preserve fertility in young cancer survivors without compromising anticancer efficacy.
Research from Nature Portfolio
No recent Nature Portfolio content available.
Cisplatin-Induced Testicular Toxicity and Protective Mechanisms publication trend
The graph below shows the total number of articles in cisplatin-induced testicular toxicity and protective mechanisms across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen metabolism that can damage cellular macromolecules.
Oxidative stress: An imbalance favouring oxidants over antioxidants, resulting in molecular and cellular injury.
Apoptosis: Programmed cell death mediated by caspases, leading to organised dismantling of cellular components.
Spermatogenesis: The process of sperm cell development from spermatogonial stem cells through meiosis and differentiation.
Leydig cells: Interstitial cells in the testis responsible for testosterone synthesis under luteinising hormone stimulation.
Sertoli cells: Somatic cells that support germ cell development and maintain the blood–testis barrier.
Nrf2 pathway: A cellular defence mechanism in which the transcription factor Nrf2 induces antioxidant and cytoprotective gene expression.
Autophagy: A lysosome‐dependent process that degrades and recycles damaged organelles and proteins to maintain cellular homeostasis.
References
- Nme8 is essential for protection against chemotherapy drug cisplatin-induced male reproductive toxicity in mice. Cell Death & Disease (2024).
- Mechanistic Protective Effect of Cilostazol in Cisplatin-Induced Testicular Damage via Regulation of Oxidative Stress and TNF-α/NF-κB/Caspase-3 Pathways. International Journal of Molecular Sciences (2023).
- Cisplatin-induced azoospermia and testicular damage ameliorated by adipose-derived mesenchymal stem cells. Biological Research (2023).
About these summaries
This Nature Research Intelligence Topic summary is created with the cited references and a large language model. We take care to ground generated text with facts, and have systems in place to gain human feedback on the overall quality of the process in line with our AI principles. We strive to create accurate and useful summaries for people unfamiliar with the research topic and that supports this goal. These pages are a beta release and will be updated as we learn how best to help people gain value from a research topic summary.
Turn complex research questions into confident strategic decisions
When you're under pressure to set direction, justify investment, or understand your competitive position, you need more than raw data — you need trusted insights you can act on.
Benchmark your performance against global peers using robust, methodologically sound analysis.
Combine quantitative metrics with qualitative expert insight to uncover strengths, gaps and emerging opportunities.
Gain tailored, decision-ready recommendations aligned to your strategic priorities.
Talk to us to learn more about our data dashboards and bespoke strategy reports.
Grow research skills, confidence and careers with training built for every stage of the research lifecycle.
Developed with Nature Portfolio journal Editors and internationally renowned experts. Discover three ways to learn:
Self-paced, online courses in convenient bite-sized units, covering key skills across scientific writing, publishing, grant writing, data analysis, and more.
Expert trainer-led workshops with hands-on exercises and real-time feedback across core research skills, delivered via interactive group sessions.
Editor-led workshops combining core principles in writing and publishing, personalised 1:1 feedback from Nature Portfolio Editors and hands-on exercises.
Explore course catalogues and workshop agendas, enquire about the options or request institutional pricing.