ArticleScientific reports2026
Thymoquinone attenuates tricyclazole-induced testicular dysfunction through endocrine, redox, histomorphometric and sperm function changes in rats.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Male infertility is increasingly linked to environmental toxicants that perturb redox and endocrine homeostasis. Thymoquinone, a bioactive quinone with antioxidant, anti-inflammatory, and mitochondrial-stabilizing properties, may protect the seminiferous epithelium from such insults. Here, we tested whether thymoquinone attenuates tricyclazole-induced testicular injury across endocrine, redox, structural, molecular, and functional endpoints in adult rats assigned to four groups: Vehicle, tricyclazole, thymoquinone, and tricyclazole plus thymoquinone for 58 days. An integrated workflow combined serum testosterone and gonadosomatic index with testicular oxidative-stress biomarkers, qualitative histopathology, quantitative histomorphometry, spermatogenesis indices, stage-resolved transcript profiling, and epididymal sperm assessment using computer-assisted motion analysis and eosin-nigrosin viability staining. Tricyclazole reduced testosterone and gonadosomatic index, increased lipid peroxidation, suppressed superoxide dismutase activity, and disrupted seminiferous architecture, with epithelial thinning, vacuolization, germ-cell sloughing, and luminal enlargement. It also reduced differentiation and late maturation indices, whereas the repopulation index remained largely preserved, indicating that early spermatogonial repopulation was not detectably impaired under the present exposure conditions. In parallel, tricyclazole produced stage-resolved transcriptional suppression across selected pre-meiotic, meiotic, and post-meiotic markers, suggesting downstream disruption of spermatogenic progression rather than uniform impairment of all spermatogenic compartments. Thymoquinone alone was comparable to Vehicle across most endpoints. Co-treatment produced coherent but incomplete attenuation, improving endocrine and redox status, shifting epithelial organization, luminal geometry, transcript levels, and sperm performance toward baseline without full normalization. These data support thymoquinone as a pharmacognostically relevant protective compound against pesticide-associated male reproductive toxicity and justify dose optimization, steroidogenic profiling, and fertility-confirmation studies.
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