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Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model
Background and Aim Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury. Materials and...
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| Published in: | Birth defects research 2024-02, Vol.116 (2), p.e2315-n/a |
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| container_title | Birth defects research |
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| creator | Gholami, Mohammadreza Nemati, Afsaneh Zarasvand, Azita Alasvand Zendehdel, Abolfazl Jalili, Cyrus Rashidi, Iraj Mansouri, Kamran Taheri, Forough Assadollahi, Vahideh Gholami, Elham |
| description | Background and Aim
Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury.
Materials and Methods
Male mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle‐stimulating hormone (FSH) levels. Real‐time quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B‐cell lymphoma 2 (Bcl2), and Bcl2‐associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p |
| doi_str_mv | 10.1002/bdr2.2315 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2926079531</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2932656595</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3135-e03cd4efa54b14a290dad90a683781b958e1b58b2f86072bd6194e3658e45f253</originalsourceid><addsrcrecordid>eNp1kMlOwzAQhi0EolXhwAugSFzgUPASJw43KFslFonlbDnxpHWVpdiJoDcegWfkSXBoQQiJk8f2N9-MfoR2CD4kGNOjVFt6SBnha6hPw5gOSUzj9V91D207N8MYE0FJzMQm6jHBQhGFvI_kAxRQmbYMStOYiWrABSU007qx8OpvH2_vptJtBjrwX43J2kLZwFSz1i6Og3HlzGTauCC3tTeoAoLbm_uxd2UQlLWGYgtt5KpwsL06B-jp4vxxdDW8vrscj06uhxkjjA8Bs0yHkCsepiRUNMFa6QSrSLBYkDThAkjKRUpzEeGYpjoiSQgs8u8hzylnA7S_9M5t_dz6TWVpXAZFoSqoWydpQn1jwv20Adr7g87q1lZ-O08xGvGIJ53wYElltnbOQi7n1pTKLiTBsgtedsHLLnjP7q6MbVqC_iG_Y_bA0RJ4MQUs_jfJ07N7-qX8BN0ZjJc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2932656595</pqid></control><display><type>article</type><title>Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model</title><source>Wiley</source><creator>Gholami, Mohammadreza ; Nemati, Afsaneh ; Zarasvand, Azita Alasvand ; Zendehdel, Abolfazl ; Jalili, Cyrus ; Rashidi, Iraj ; Mansouri, Kamran ; Taheri, Forough ; Assadollahi, Vahideh ; Gholami, Elham</creator><creatorcontrib>Gholami, Mohammadreza ; Nemati, Afsaneh ; Zarasvand, Azita Alasvand ; Zendehdel, Abolfazl ; Jalili, Cyrus ; Rashidi, Iraj ; Mansouri, Kamran ; Taheri, Forough ; Assadollahi, Vahideh ; Gholami, Elham</creatorcontrib><description>Background and Aim
Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury.
Materials and Methods
Male mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle‐stimulating hormone (FSH) levels. Real‐time quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B‐cell lymphoma 2 (Bcl2), and Bcl2‐associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p < .05).
Results
Histopathological analysis revealed significant testicular damage in the MTX group, with decreased spermatogenesis and Leydig cell count, while Se administration mitigated these effects, preserving the structural integrity of the reproductive epithelium. Biochemical analysis demonstrated that MTX led to elevated malondialdehyde (MDA) levels and reduced testosterone, LH, and FSH levels, suggesting oxidative stress and Leydig cell dysfunction. Gene expression analysis indicated that MTX upregulated proapoptotic genes (casp3, p53, and bax) while downregulating the antiapoptotic Bcl2 gene. In contrast, Se treatment reversed these trends, highlighting its potential antiapoptotic properties.
Conclusion
Our findings underscore the potential of Se as a therapeutic agent to mitigate the reproductive toxicity associated with MTX‐induced testicular injury. Se exerts protective effects by regulating oxidative stress, preserving hormone balance, and modulating apoptotic pathways. These results suggest that Se supplementation could be a promising strategy to alleviate chemotherapy‐induced testicular damage and preserve male fertility.</description><identifier>ISSN: 2472-1727</identifier><identifier>EISSN: 2472-1727</identifier><identifier>DOI: 10.1002/bdr2.2315</identifier><identifier>PMID: 38348645</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Animals ; Apoptosis ; BAX protein ; Bcl-2 protein ; bcl-2-Associated X Protein - metabolism ; Bcl-x protein ; Biochemical analysis ; Biochemical tests ; Biopsy ; Caspase 3 - metabolism ; Caspase-3 ; Chemotherapy ; Damage ; Epithelium ; Fertility ; Follicle Stimulating Hormone ; Gene expression ; Genes ; Injuries ; Luteinizing hormone ; Luteinizing Hormone - metabolism ; Lymphoma ; Male ; male reproduction ; Males ; Malondialdehyde ; Malondialdehyde - metabolism ; Methotrexate ; Methotrexate - adverse effects ; Mice ; Oxidative stress ; p53 Protein ; Pharmacology ; Polymerase chain reaction ; Proteins ; Selenium ; Selenium - pharmacology ; Spermatogenesis ; Statistical analysis ; Structural integrity ; Testes ; Testosterone ; Toxicity ; Tumor Suppressor Protein p53 ; Variance analysis</subject><ispartof>Birth defects research, 2024-02, Vol.116 (2), p.e2315-n/a</ispartof><rights>2024 Wiley Periodicals LLC.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3135-e03cd4efa54b14a290dad90a683781b958e1b58b2f86072bd6194e3658e45f253</cites><orcidid>0000-0001-9623-1986 ; 0000-0003-3871-807X ; 0000-0003-3719-1659</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38348645$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gholami, Mohammadreza</creatorcontrib><creatorcontrib>Nemati, Afsaneh</creatorcontrib><creatorcontrib>Zarasvand, Azita Alasvand</creatorcontrib><creatorcontrib>Zendehdel, Abolfazl</creatorcontrib><creatorcontrib>Jalili, Cyrus</creatorcontrib><creatorcontrib>Rashidi, Iraj</creatorcontrib><creatorcontrib>Mansouri, Kamran</creatorcontrib><creatorcontrib>Taheri, Forough</creatorcontrib><creatorcontrib>Assadollahi, Vahideh</creatorcontrib><creatorcontrib>Gholami, Elham</creatorcontrib><title>Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model</title><title>Birth defects research</title><addtitle>Birth Defects Res</addtitle><description>Background and Aim
Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury.
Materials and Methods
Male mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle‐stimulating hormone (FSH) levels. Real‐time quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B‐cell lymphoma 2 (Bcl2), and Bcl2‐associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p < .05).
Results
Histopathological analysis revealed significant testicular damage in the MTX group, with decreased spermatogenesis and Leydig cell count, while Se administration mitigated these effects, preserving the structural integrity of the reproductive epithelium. Biochemical analysis demonstrated that MTX led to elevated malondialdehyde (MDA) levels and reduced testosterone, LH, and FSH levels, suggesting oxidative stress and Leydig cell dysfunction. Gene expression analysis indicated that MTX upregulated proapoptotic genes (casp3, p53, and bax) while downregulating the antiapoptotic Bcl2 gene. In contrast, Se treatment reversed these trends, highlighting its potential antiapoptotic properties.
Conclusion
Our findings underscore the potential of Se as a therapeutic agent to mitigate the reproductive toxicity associated with MTX‐induced testicular injury. Se exerts protective effects by regulating oxidative stress, preserving hormone balance, and modulating apoptotic pathways. These results suggest that Se supplementation could be a promising strategy to alleviate chemotherapy‐induced testicular damage and preserve male fertility.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Bcl-x protein</subject><subject>Biochemical analysis</subject><subject>Biochemical tests</subject><subject>Biopsy</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Chemotherapy</subject><subject>Damage</subject><subject>Epithelium</subject><subject>Fertility</subject><subject>Follicle Stimulating Hormone</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Injuries</subject><subject>Luteinizing hormone</subject><subject>Luteinizing Hormone - metabolism</subject><subject>Lymphoma</subject><subject>Male</subject><subject>male reproduction</subject><subject>Males</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Methotrexate</subject><subject>Methotrexate - adverse effects</subject><subject>Mice</subject><subject>Oxidative stress</subject><subject>p53 Protein</subject><subject>Pharmacology</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Selenium</subject><subject>Selenium - pharmacology</subject><subject>Spermatogenesis</subject><subject>Statistical analysis</subject><subject>Structural integrity</subject><subject>Testes</subject><subject>Testosterone</subject><subject>Toxicity</subject><subject>Tumor Suppressor Protein p53</subject><subject>Variance analysis</subject><issn>2472-1727</issn><issn>2472-1727</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kMlOwzAQhi0EolXhwAugSFzgUPASJw43KFslFonlbDnxpHWVpdiJoDcegWfkSXBoQQiJk8f2N9-MfoR2CD4kGNOjVFt6SBnha6hPw5gOSUzj9V91D207N8MYE0FJzMQm6jHBQhGFvI_kAxRQmbYMStOYiWrABSU007qx8OpvH2_vptJtBjrwX43J2kLZwFSz1i6Og3HlzGTauCC3tTeoAoLbm_uxd2UQlLWGYgtt5KpwsL06B-jp4vxxdDW8vrscj06uhxkjjA8Bs0yHkCsepiRUNMFa6QSrSLBYkDThAkjKRUpzEeGYpjoiSQgs8u8hzylnA7S_9M5t_dz6TWVpXAZFoSqoWydpQn1jwv20Adr7g87q1lZ-O08xGvGIJ53wYElltnbOQi7n1pTKLiTBsgtedsHLLnjP7q6MbVqC_iG_Y_bA0RJ4MQUs_jfJ07N7-qX8BN0ZjJc</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Gholami, Mohammadreza</creator><creator>Nemati, Afsaneh</creator><creator>Zarasvand, Azita Alasvand</creator><creator>Zendehdel, Abolfazl</creator><creator>Jalili, Cyrus</creator><creator>Rashidi, Iraj</creator><creator>Mansouri, Kamran</creator><creator>Taheri, Forough</creator><creator>Assadollahi, Vahideh</creator><creator>Gholami, Elham</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9623-1986</orcidid><orcidid>https://orcid.org/0000-0003-3871-807X</orcidid><orcidid>https://orcid.org/0000-0003-3719-1659</orcidid></search><sort><creationdate>202402</creationdate><title>Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model</title><author>Gholami, Mohammadreza ; Nemati, Afsaneh ; Zarasvand, Azita Alasvand ; Zendehdel, Abolfazl ; Jalili, Cyrus ; Rashidi, Iraj ; Mansouri, Kamran ; Taheri, Forough ; Assadollahi, Vahideh ; Gholami, Elham</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3135-e03cd4efa54b14a290dad90a683781b958e1b58b2f86072bd6194e3658e45f253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Bcl-x protein</topic><topic>Biochemical analysis</topic><topic>Biochemical tests</topic><topic>Biopsy</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Chemotherapy</topic><topic>Damage</topic><topic>Epithelium</topic><topic>Fertility</topic><topic>Follicle Stimulating Hormone</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Injuries</topic><topic>Luteinizing hormone</topic><topic>Luteinizing Hormone - metabolism</topic><topic>Lymphoma</topic><topic>Male</topic><topic>male reproduction</topic><topic>Males</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Methotrexate</topic><topic>Methotrexate - adverse effects</topic><topic>Mice</topic><topic>Oxidative stress</topic><topic>p53 Protein</topic><topic>Pharmacology</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Selenium</topic><topic>Selenium - pharmacology</topic><topic>Spermatogenesis</topic><topic>Statistical analysis</topic><topic>Structural integrity</topic><topic>Testes</topic><topic>Testosterone</topic><topic>Toxicity</topic><topic>Tumor Suppressor Protein p53</topic><topic>Variance analysis</topic><toplevel>online_resources</toplevel><creatorcontrib>Gholami, Mohammadreza</creatorcontrib><creatorcontrib>Nemati, Afsaneh</creatorcontrib><creatorcontrib>Zarasvand, Azita Alasvand</creatorcontrib><creatorcontrib>Zendehdel, Abolfazl</creatorcontrib><creatorcontrib>Jalili, Cyrus</creatorcontrib><creatorcontrib>Rashidi, Iraj</creatorcontrib><creatorcontrib>Mansouri, Kamran</creatorcontrib><creatorcontrib>Taheri, Forough</creatorcontrib><creatorcontrib>Assadollahi, Vahideh</creatorcontrib><creatorcontrib>Gholami, Elham</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Birth defects research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gholami, Mohammadreza</au><au>Nemati, Afsaneh</au><au>Zarasvand, Azita Alasvand</au><au>Zendehdel, Abolfazl</au><au>Jalili, Cyrus</au><au>Rashidi, Iraj</au><au>Mansouri, Kamran</au><au>Taheri, Forough</au><au>Assadollahi, Vahideh</au><au>Gholami, Elham</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model</atitle><jtitle>Birth defects research</jtitle><addtitle>Birth Defects Res</addtitle><date>2024-02</date><risdate>2024</risdate><volume>116</volume><issue>2</issue><spage>e2315</spage><epage>n/a</epage><pages>e2315-n/a</pages><issn>2472-1727</issn><eissn>2472-1727</eissn><abstract>Background and Aim
Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury.
Materials and Methods
Male mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle‐stimulating hormone (FSH) levels. Real‐time quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B‐cell lymphoma 2 (Bcl2), and Bcl2‐associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p < .05).
Results
Histopathological analysis revealed significant testicular damage in the MTX group, with decreased spermatogenesis and Leydig cell count, while Se administration mitigated these effects, preserving the structural integrity of the reproductive epithelium. Biochemical analysis demonstrated that MTX led to elevated malondialdehyde (MDA) levels and reduced testosterone, LH, and FSH levels, suggesting oxidative stress and Leydig cell dysfunction. Gene expression analysis indicated that MTX upregulated proapoptotic genes (casp3, p53, and bax) while downregulating the antiapoptotic Bcl2 gene. In contrast, Se treatment reversed these trends, highlighting its potential antiapoptotic properties.
Conclusion
Our findings underscore the potential of Se as a therapeutic agent to mitigate the reproductive toxicity associated with MTX‐induced testicular injury. Se exerts protective effects by regulating oxidative stress, preserving hormone balance, and modulating apoptotic pathways. These results suggest that Se supplementation could be a promising strategy to alleviate chemotherapy‐induced testicular damage and preserve male fertility.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>38348645</pmid><doi>10.1002/bdr2.2315</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-9623-1986</orcidid><orcidid>https://orcid.org/0000-0003-3871-807X</orcidid><orcidid>https://orcid.org/0000-0003-3719-1659</orcidid></addata></record> |
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| subjects | Animals Apoptosis BAX protein Bcl-2 protein bcl-2-Associated X Protein - metabolism Bcl-x protein Biochemical analysis Biochemical tests Biopsy Caspase 3 - metabolism Caspase-3 Chemotherapy Damage Epithelium Fertility Follicle Stimulating Hormone Gene expression Genes Injuries Luteinizing hormone Luteinizing Hormone - metabolism Lymphoma Male male reproduction Males Malondialdehyde Malondialdehyde - metabolism Methotrexate Methotrexate - adverse effects Mice Oxidative stress p53 Protein Pharmacology Polymerase chain reaction Proteins Selenium Selenium - pharmacology Spermatogenesis Statistical analysis Structural integrity Testes Testosterone Toxicity Tumor Suppressor Protein p53 Variance analysis |
| title | Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model |
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