ArticleScientific reports2024
Therapeutic effect of sodium alginate on bleomycin, etoposide and cisplatin (BEP)-induced reproductive toxicity by inhibiting nitro-oxidative stress, inflammation and apoptosis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 16 citations in OpenAlex.
- Selenoprotein H targets MTCH2 to regulate MFN2-dependent mitochondrial quality control to alleviate acute kidney injury.Journal of advanced research · 2026Article
- Arab gum coating enhances the bioavailability and therapeutic potential of nanoselenium in cisplatin-induced testicular toxicity.Scientific reports · 2026Article
- L-Proline supplementation preserves sperm function and chromatin integrity in asthenozoospermic patients during cryopreservation.Basic and clinical andrology · 2025Article
- Therapeutic potential of heat-killed Lactobacillus reuteri against bile acid-induced male reproductive toxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Medical Ozone Treatment Attenuates Male Reproductive Toxicity Induced by Bleomycin, Etoposide, and Cisplatin Regimen in an Experimental Animal Model.International journal of molecular sciences · 2025Article
- Carob extract restores testicular function and sperm quality in cadmium-exposed mice: An experimental study.International journal of reproductive biomedicine · 2025Article
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7 authors at 2 institutions in 1 country.
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Abstract
Impaired spermatogenesis and male infertility are common consequences of chemotherapy drugs used in patients with testicular cancer. The present study investigated the effects of sodium alginate (NaAL) on testicular toxicity caused by bleomycin, etoposide, and cisplatin (BEP). Rats in group 1 received normal saline, while groups 2 and 3 were treated with 25 and 50 mg/kg of NaAL, respectively. Group 4 was treated with a 21-day cycle of BEP (0.5 mg/kg bleomycin, 5 mg/kg etoposide, and 1 mg/kg cisplatin), and groups 5 and 6 received BEP regimen plus 25 and 50 mg/kg of NaAL, respectively. Then, sperm parameters, testosterone levels, testicular histopathology and stereological parameters, testicular levels of malondialdehyde (MDA), nitric oxide (NO), and total antioxidant capacity (TAC), and the expression of apoptosis-associated genes including Bcl2, Bax, Caspase3, p53, and TNF-α were evaluated. Our findings revealed that NaAL improved sperm parameters, testosterone levels, histopathology, and stereology parameters in BEP-administrated rats. NaAL also improved testis antioxidant status by enhancing TAC and ameliorating MDA and NO. Further, modifications to the expression of Bcl2, Bax, Caspase3, p53, and TNF-α suggested that NaAL alleviated BEP-induced apoptosis and inflammation. Collectively, NaAL protects rats' testes against BEP-evoked toxicity damage through the modulation of nitro-oxidative stress, apoptosis, and inflammation.
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