ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Telmisartan ameliorates reproductive dysfunction, oxidative stress, and mitochondrial damages induced by fipronil in male rats via regulation of Nrf2/HO-1/PGC-1α/MNF2/DRP1.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
Fipronil (FIP), as a broad-spectrum pesticide, contributes to adverse reproductive effects. Thus, our study aimed to investigate the effect of telmisartan (TEL) as a selective angiotensin 1 receptor (AT1R) blocker on mitochondrial damage induced by FIP intoxication in male rats. Forty healthy male albino rats were allocated into 4 groups (10/ group): the control group, the TEL group received TEL (10 mg/kg b.wt.), the FIP group received FIP (1/10 of the LD50 of 97 mg/kg b.wt.), and the FIP + TEL cotreated group. All treatments were taken orally for 60 days. Before the experiment, in-silico assessments of FIP and TEL were done. FIP administration diminished relative testicular weight, sperm count, and motility, besides significantly increasing sperm abnormalities (p < 0.05). Biochemically, FIP treatment reduced considerably (p < 0.05) serum testosterone, luteinizing hormone (LH), and follicular-stimulating hormone (FSH) levels related to control animals. Furthermore, FIP administration significantly increased testicular malondialdehyde (MDA), pro-inflammatory markers as tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) levels. Also, downregulated the activities of antioxidant markers, Nrf2, HO-1, and PCNA immunostaining. Furthermore, FIP significantly upregulated (p < 0.05) DRP1 and downregulated PGC-1α, MNF2, TFAM, and mtDNA mRNA transcripts. Histopathologically, FIP induced deterioration in seminiferous tubules' histoarchitecture with upregulation in Cosentino's score and downregulation in Johnson's score. On the contrary, TEL effectively restored the testicular function hormones, testicular and epididymal histoarchitecture, antioxidant indices, PGC-1α, and TFAM, with downregulation in MDA levels and DRP1 mRNA transcript. In conclusion, TEL protects the testicular mitochondria against damage from FIP toxicosis by modulating the Nrf2/HO-1/PGC-1α/MNF2/DRP1 expressions.
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