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Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats

INTRODUCTION: Zonisamide (ZNS) is a modern antiepileptic drug (AED) that is distinguished from other AEDs by its unique structure and broad mechanistic profile. The pineal hormone melatonin is involved in the regulation of reproductive function, including the timing of the luteinizing hormone (LH) s...

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Autores principales: Khalil, Wagdy K.B., Abdu, Faiza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495141/
https://www.ncbi.nlm.nih.gov/pubmed/26170862
http://dx.doi.org/10.5114/aoms.2013.39384
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author Khalil, Wagdy K.B.
Abdu, Faiza
author_facet Khalil, Wagdy K.B.
Abdu, Faiza
author_sort Khalil, Wagdy K.B.
collection PubMed
description INTRODUCTION: Zonisamide (ZNS) is a modern antiepileptic drug (AED) that is distinguished from other AEDs by its unique structure and broad mechanistic profile. The pineal hormone melatonin is involved in the regulation of reproductive function, including the timing of the luteinizing hormone (LH) surge. The aim of the present work was to study the protective effect of melatonin against the potential suppression impact of ZNS on reproductive activity. MATERIAL AND METHODS: Ninety adult albino male rats were allocated to several groups treated with melatonin (10 mg/kg BW), ZNS (10, 20 and 50 mg/kg BW) and 10 mg/kg of melatonin plus ZNS (10, 20 or 50 mg/kg BW, respectively). Reproductive hormones (testosterone, LH and follicle-stimulating hormone (FSH)) levels were measured in animal serum. Sperm abnormalities and DNA fragmentation in testis tissues as well as expression alteration of several reproductive-related genes were analyzed. RESULTS: The results revealed that ZNS decreased the levels of serum free testosterone, LH, and FSH and expression of their encoding genes in male rats. In addition, ZNS treatment increased the sperm abnormalities and DNA fragmentation and inducible nitric oxide synthase (iNOS) in testis tissues as well as GABA level in liver tissues. However, melatonin supplementation inhibited the negative symptoms of ZNS in which it increased the levels of reproductive hormones and expression of their encoding genes in the ZNS-treated rats. Moreover, melatonin decreased the sperm abnormalities, DNA fragmentation, iNOS activity and GABA level in ZNS-treated rats. CONCLUSIONS: The data obtained in this study suggest that melatonin administration confers protection against toxicity inflicted by ZNS, and support the contention that melatonin protection is achieved by its ability as a scavenger for free radicals generated by ZNS.
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spelling pubmed-44951412015-07-13 Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats Khalil, Wagdy K.B. Abdu, Faiza Arch Med Sci Experimental Research INTRODUCTION: Zonisamide (ZNS) is a modern antiepileptic drug (AED) that is distinguished from other AEDs by its unique structure and broad mechanistic profile. The pineal hormone melatonin is involved in the regulation of reproductive function, including the timing of the luteinizing hormone (LH) surge. The aim of the present work was to study the protective effect of melatonin against the potential suppression impact of ZNS on reproductive activity. MATERIAL AND METHODS: Ninety adult albino male rats were allocated to several groups treated with melatonin (10 mg/kg BW), ZNS (10, 20 and 50 mg/kg BW) and 10 mg/kg of melatonin plus ZNS (10, 20 or 50 mg/kg BW, respectively). Reproductive hormones (testosterone, LH and follicle-stimulating hormone (FSH)) levels were measured in animal serum. Sperm abnormalities and DNA fragmentation in testis tissues as well as expression alteration of several reproductive-related genes were analyzed. RESULTS: The results revealed that ZNS decreased the levels of serum free testosterone, LH, and FSH and expression of their encoding genes in male rats. In addition, ZNS treatment increased the sperm abnormalities and DNA fragmentation and inducible nitric oxide synthase (iNOS) in testis tissues as well as GABA level in liver tissues. However, melatonin supplementation inhibited the negative symptoms of ZNS in which it increased the levels of reproductive hormones and expression of their encoding genes in the ZNS-treated rats. Moreover, melatonin decreased the sperm abnormalities, DNA fragmentation, iNOS activity and GABA level in ZNS-treated rats. CONCLUSIONS: The data obtained in this study suggest that melatonin administration confers protection against toxicity inflicted by ZNS, and support the contention that melatonin protection is achieved by its ability as a scavenger for free radicals generated by ZNS. Termedia Publishing House 2013-12-05 2015-06-19 /pmc/articles/PMC4495141/ /pubmed/26170862 http://dx.doi.org/10.5114/aoms.2013.39384 Text en Copyright © 2015 Termedia & Banach http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Experimental Research
Khalil, Wagdy K.B.
Abdu, Faiza
Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title_full Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title_fullStr Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title_full_unstemmed Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title_short Protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
title_sort protective effect of melatonin against zonisamide-induced reproductive disorders in male rats
topic Experimental Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495141/
https://www.ncbi.nlm.nih.gov/pubmed/26170862
http://dx.doi.org/10.5114/aoms.2013.39384
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