<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-28T20:38:30Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/32374" metadataPrefix="marc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/32374</identifier><datestamp>2026-02-03T11:30:51Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Romero-Zerbo, Silvana Yanina</subfield>
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      <subfield code="a">Decara, Juan</subfield>
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      <subfield code="a">El Bekay Rizky, Rajaa</subfield>
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      <subfield code="a">Sánchez-Salido, Lourdes</subfield>
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      <subfield code="a">Del Arco-Herrera, Ignacio</subfield>
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      <subfield code="a">Rodriguez-de-Fonseca, Fernando</subfield>
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      <subfield code="a">De-Diego-Otero, María Yolanda</subfield>
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      <subfield code="c">2009</subfield>
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      <subfield code="a">Fragile X syndrome is the most common form of inherited mentalretardation. It is typically caused by a mutation of the Fragile X mental-retardation 1 (Fmr1) gene. To better understand the role of the Fmr1 geneand its gene product, the fragile X mental-retardation protein in centralnervous system functions, an fmr1 knockout mouse that is deﬁcient in thefragile X mental-retardation protein was bred. In the present study, fragile Xmental retardation 1-knockout and wild-type mice are used to determinebehaviour and oxidative stress alterations, including reduced glutathione,oxidized glutathione and thiobarbituric acid-reactive substances, before andafter chronic treatment with melatonin or tianeptine. Reduced glutathionelevels were reduced in the brain of fmr1-knockout mice and chronicmelatonin treatment normalized the glutathione levels compared withthe control group. Lipid peroxidation was elevated in brain and testes offmr1-knockout mice and chronic melatonin treatment prevents lipidperoxidation in both tissues. Interestingly, chronic treatment with melatoninalleviated the altered parameters in the fmr1-knockout mice, includingabnormal context-dependent exploratory and anxiety behaviours andlearning abnormalities. Chronic treatment with tianeptine (a serotoninreuptake enhancer) did not normalize the behaviour in fmr1-knockout mice.The prevention of oxidative stress in the fragile X mouse model, by anantioxidant compound such as melatonin, emerges as a new and promisingapproach for further investigation on treatment trials for the disease</subfield>
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      <subfield code="a">Romero-Zerbo, Y., Decara, J., El Bekay, R., Sanchez-Salido, L., Del Arco-Herrera, I., De Fonseca, F.R. and De Diego-Otero, Y. (2009), Protective effects of melatonin against oxidative stress in Fmr1 knockout mice: a therapeutic research model for the fragile X syndrome. Journal of Pineal Research, 46: 224-234. https://doi.org/10.1111/j.1600-079X.2008.00653.x</subfield>
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      <subfield code="a">https://hdl.handle.net/10630/32374</subfield>
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      <subfield code="a">10.1111/j.1600-079X.2008.00653.x</subfield>
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      <subfield code="a">Melatonina</subfield>
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      <subfield code="a">Sistema nervioso central</subfield>
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      <subfield code="a">Estrés oxidativo</subfield>
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      <subfield code="a">Protective effects of melatonin against oxidative stress in Fmr1 knockout mice: a therapeutic research model for the fragile X syndrome</subfield>
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