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Assessing reproductive toxicity and antioxidant enzymes on beta asarone induced male Wistar albino rats: In vivo and computational analysis
Published in Elsevier BV
PMID: 27569590
Volume: 173
Pages: 150 - 160
Aim Beta asarone is the major constituent of oil obtained from Acorus calamus, the Indian traditional medicine plant. Several studies have shown that beta asarone causes liver and cardiac damages but the reproductive toxicity is not well understood. The present study was initiated to investigate whether beta asarone has the potential to cause reproductive toxicity by inducing oxidative stress in the testis of male Wistar albino rats. Materials and methods For this study, the animals were divided into six groups: Group I was treated with saline (normal saline), Group II with DMSO (vehicle control) and Group III with cisplatin (10 mg/kg b.wt.). Group IV, V and VI animals were administrated at three dose levels of beta asarone 12.5, 25 and 50 mg/kg b.wt. The treatment was carried out for 14 days and animals were sacrificed on 29th day and processed for sperm analysis, hormone assay, histopathological, and antioxidant enzymatic assays. We also used molecular docking studies to predict the binding nature of beta asarone with luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). Key findings Beta asarone administered at a dose of 50 mg/kg b.wt. was responsible for inducing certain noticeable degenerative changes in histopathological analysis of the tissue. This was supported by altered sperm morphology and hormonal variations when compared to the control groups. Antioxidant enzyme levels were also found to be decreased. This was further validated by molecular docking studies. Significance The present study provides evidence that beta asarone administered at a dose of 50 mg/kg b.wt. is capable enough in bringing about moderate amount of degenerative changes in rat testis and altered antioxidant status. Therefore provides a suitable evidence to prove that beta asarone causes reproductive toxicity. © 2016 Elsevier Inc.
About the journal
JournalData powered by TypesetLife Sciences
PublisherData powered by TypesetElsevier BV
Open AccessNo
Authors (3)