Reproductive Toxicity of Nonsteroidal Anti-Inflammatory Drugs in Male Models
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) constitute one of the most widely employed pharmacological classes worldwide, with extensive use in pain management, fever reduction and inflammatory disorders. In male experimental models, NSAID exposure has been shown to disrupt testicular function through inhibition of cyclooxygenase enzymes, perturbation of eicosanoid signalling and induction of oxidative stress within the gonad. These alterations manifest as impaired spermatogenesis, reduced sperm motility and morphology abnormalities, alongside endocrine disturbances including suppressed testosterone synthesis and altered luteinising hormone–follicle-stimulating hormone balance. Pre- and perinatal administration of NSAIDs may additionally compromise testicular development by affecting germ cell proliferation and Sertoli cell support functions, potentially resulting in long-term deficits in sperm production. The breadth of these findings underscores the need for judicious NSAID use in populations at risk of reproductive impairment and highlights avenues for protective interventions.
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Reproductive Toxicity of Nonsteroidal Anti-Inflammatory Drugs in Male Models publication trend
The graph below shows the total number of articles in reproductive toxicity of nonsteroidal anti-inflammatory drugs in male models across all publications each year (not limited to Nature Index journals).
Technical terms
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): A class of analgesic and anti-inflammatory agents that inhibit cyclooxygenase enzymes to reduce prostaglandin synthesis.
Cyclooxygenase (COX): Enzymes (COX-1 and COX-2) responsible for the conversion of arachidonic acid into prostaglandins and thromboxanes.
Eicosanoids: Bioactive lipid mediators derived from arachidonic acid that regulate inflammation, vascular tone and cellular signalling in reproductive tissues.
Oxidative Stress: A state of imbalance between reactive oxygen species production and antioxidant defences, leading to cellular damage in testicular tissue.
Spermatogenesis: The multi-stage process of sperm cell development within the seminiferous tubules, reliant on precise endocrine and paracrine regulation.
References
- Eicosanoid Biosynthesis in Male Reproductive Development: Effects of Perinatal Exposure to NSAIDs and Analgesic Drugs. Frontiers in Toxicology (2022).
- Chitosan/Selenium Nanoparticles Attenuate Diclofenac Sodium-Induced Testicular Toxicity in Male Rats. Crystals (2021).
- Prostaglandin levels in seminal plasma and sperm extracts of the domestic turkey, and the effects of cyclooxygenase inhibitors on sperm mobility. Reproductive Biology and Endocrinology (2003).
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