ArticleJBRA assisted reproduction2024
The protective effect of Ozone on the mice testicular damage induced by methotrexate.
Article in JBRA assisted reproduction, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- 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
- The Relationship Between Tramadol-Induced Oxidative Testis Injury and Reproductive Function Disorder and Adenosine Triphosphate.Life (Basel, Switzerland) · 2025Article
- Low-Dose Ozone as a Eustress Inducer: Experimental Evidence of the Molecular Mechanisms Accounting for Its Therapeutic Action.International journal of molecular sciences · 2024Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMethotrexate (MTX) is widely administered for the treatment of various cancers. However, MTX induces male reproductive toxicity. In the current study, the effect of ozone therapy (OT) on reducing the toxic effects of MTX in the mouse testicles has been investigated.
methodsTwenty-four mice were divided into four groups: control, OT (4 mg/kg ozone), MTX (20 mg/kg), and MTX + OT. Testosterone levels, histological changes, and oxidative stress biomarkers were assessed to evaluate the protective effects of OT.
resultsThe results demonstrated that MTX disrupted germinal epithelium, reduced serum testosterone levels, and enhanced oxidative stress in testicular tissue. However, treatment with OT attenuated these adverse effects. OT effectively restored the levels of antioxidant enzymes, such as catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD). OT reduced lipid peroxidation, as indicated by decreased malondialdehyde (MDA) levels. OT preserved normal spermatogenesis, improved morphometric parameters, and reduced histological changes by MTX. Moreover, OT effectively restored testosterone levels.
conclusionsOT protects against MTX-induced testicular damage by suppressing oxidative stress.
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