ArticleSmall (Weinheim an der Bergstrasse, Germany)2026
Maternal Bisphenol S Exposure Impairs Testicular Development and Sperm Function in Male Offspring by Disrupting the Immune-Endocrine Network.
Article in Small (Weinheim an der Bergstrasse, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Bisphenol S (BPS), a widely used substitute for bisphenol A, is an environmental contaminant with endocrine-disrupting properties. However, the transgenerational impact of maternal BPS exposure during gestation on male offspring reproductive health and the underlying molecular mechanisms remains unknown. This study shows that gestational exposure of mice to environmentally relevant concentrations of BPS (3, 30, and 300 µg/kg) dose- and time-dependently impairs testicular development and sperm function in male offspring. Integrated transcriptomic, physiological, and molecular analyses revealed that maternal BPS exposure remodeled the testicular transcriptome and disrupted the immune-endocrine crosstalk within the testis. This disruption was characterized by the aberrant activation of immune and inflammatory pathways, including antigen presentation, concomitant suppression of steroidogenic and metabolic processes, and induction of the renin-angiotensin system. Deconvolution analysis identified loss of Leydig cells and increased Tcell infiltration, and quantitative realtime PCR validated the dysregulation of key hub genes such as Ren1, H2-D1, Naip6, Tlr1, H2-M3, Pycard, B2m, H2-Aa, Naip1, and Cd74. Notably, western blotting revealed that HLA-DPB1, a key component of the antigen presentation pathway, was significantly downregulated at the protein level in testicular tissues. Immunofluorescence co-localization with cell-specific markers defined the precise cellular localization in the testis. Collectively, these multilevel disruptions resulted in impaired seminiferous epithelial cyclicity, enhanced interstitial collagen deposition in the testes, and severe deficits in sperm motility. Our findings reveal a novel transgenerational mechanism underlying BPS-induced testicular injury and provide robust experimental evidence of the reproductive toxicity of environmentally relevant BPS in male offspring.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.