0
Meta Analysis Tier 3 Sign in to save

Quantitative analysis and toxicological mechanisms of various male infertility inducers: A network meta-analysis and pharmacological approach.

AI summary Read the abstract

This network meta-analysis of 201 rodent studies compared nine common male infertility inducers, finding that microplastics caused among the most severe impairments to sperm count and motility — on par with the chemotherapy drug cyclophosphamide. Oxidative stress emerged as a shared mechanistic pathway across all inducers, pointing to it as a key target for understanding and potentially mitigating reproductive harm from environmental exposures.

Body Systems
Study Type Review

BACKGROUND: Male infertility is a global health concern, accounting for nearly half of all infertility cases. This study evaluates the toxicological effects of key infertility inducers in rodent models and explores underlying molecular mechanisms. METHODS: A systematic review and network meta-analysis (NMA) compared nine widely studied inducers: environmental toxicants (Bisphenol-A, Lead acetate, microplastics), pharmacological agents (Cyclophosphamide, Streptozotocin, Valproic acid, Tripterygium glycosides), and metabolic/physical stressors (High-Fat Diet, heat stress). Key endpoints included sperm count, motility, morphology, testis weight, and hormone levels. Network pharmacology and enrichment analyses identified molecular pathways, focusing on oxidative stress. Clinical relevance was assessed based on mechanistic alignment with human infertility. RESULTS: A total of 201 studies involving 3412 rodents were analyzed. NMA revealed significant differences in reproductive toxicity among inducers. Cyclophosphamide, STZ, and microplastics caused the most severe impairments, reducing sperm counts to 30.08 ± 19.1, 38.13 ± 8.2, and 18.97 ± 11.1 × 10⁶/mL, and motility to 31.73 ± 6.1 %, 30.74 ± 4.1 %, and 31.32 ± 10.2 %, respectively. Overall, sperm count, motility, and testosterone decreased by 1.46-, 1.21-, and 1.16-fold. Network pharmacology identified oxidative stress-related genes (NFE2L2, SOD1, HMOX1) as common targets, with oxidative stress emerging as shared mechanistic pathways. Trend analysis (2009-2024) revealed rising research on microplastics, HFD, and Lead acetate. CONCLUSIONS: This first integrated toxicological and mechanistic analysis elucidates how diverse inducers impair male reproductive health. Oxidative stress contributes to toxicity, highlighting potential molecular targets for therapy. Findings support the translational relevance of rodent infertility models and guide risk assessment and mitigation strategies for stressors.

More Papers Like This

Meta Analysis Tier 1

A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals

AI summary Read the abstract

This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.

Article Tier 2

Analyzing the toxicological effects of PET-MPs on male infertility: Insights from network toxicology, mendelian randomization, and transcriptomics

AI summary Read the abstract

Using network toxicology, Mendelian randomisation, and transcriptomic analysis, researchers identified mechanisms by which PET microplastics may impair male fertility, linking shared gene targets to testicular oxidative stress, hormonal disruption, and spermatogenesis interference. The multi-evidence approach strengthens the case for a causal role of PET-MP exposure in male infertility.

Article

The Impact of Microplastics on Male Fertility

AI summary Read the abstract

Microplastics and nanoplastics accumulate in testicular tissue and disrupt spermatogenesis through oxidative stress, inflammation, endocrine disruption, and structural damage to reproductive cells, consistently impairing sperm quality in experimental models. With global plastic production accelerating alongside documented declines in semen quality, this review highlights microplastic exposure as a plausible environmental contributor to male infertility warranting urgent human study.

Article Tier 2

Microplastics and impaired male reproductive health—exploring biological pathways of harm: a narrative review

AI summary Read the abstract

This narrative review summarizes the evidence that microplastics may harm male reproductive health through oxidative stress, hormone disruption, inflammation, and direct damage to reproductive cells. While animal studies show concerning effects on sperm quality, testicular function, and fertility, human studies are still lacking. The review calls for urgent research on microplastic impacts on human male fertility and for policies to reduce microplastic exposure.

Systematic Review Tier 1

Plastics in human reproductive tissues: A systematic review of detection, characterization, and effects on fertility.

AI summary Read the abstract

This review summarizes 41 studies on tiny plastic particles found in human reproductive tissues, including semen, testis, follicular fluid, and placenta. These particles were linked to cell stress, metabolic changes, and in some studies, poor sperm motility, though effects on ovarian markers and fertility outcomes were inconsistent across studies.

Research digests by email

When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.

Email me about

Share this paper