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Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria‐dependent apoptosis
The present experimental study was carried out to investigate the crosslink between aflatoxin B1 (AFB1)‐induced oxidative stress and mitochondria‐dependent apoptosis in testicles. For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was diss...
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| Published in: | Environmental toxicology 2018-11, Vol.33 (11), p.1204-1213 |
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| cites | cdi_FETCH-LOGICAL-c3907-fcbeef9a6d2ac826d8bda57f6fbf2079e8bc75a034cf68b0e5be4db103f9c4a33 |
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| creator | Yasin, Malekzadeh Mazdak, Razi Mino, Ilkhanipour |
| description | The present experimental study was carried out to investigate the crosslink between aflatoxin B1 (AFB1)‐induced oxidative stress and mitochondria‐dependent apoptosis in testicles. For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was dissolved in corn oil and ethanol (95:5, v/v) vehicle. The animals in test group subdivided into three groups, which received the AFB1 at a daily dose of 20 μg/kg body weight, through intraperitoneal (i.p.) route, for 7, 14, and 21 days. The mice in the control group received the vehicle alone for 21 days. The expression of Bcl‐2, Bax, p53, and caspase‐3 at both mRNA and protein levels were analyzed by using reverse transcription PCR (RT‐PCR) and immunohistochemistry, respectively. Moreover, the mitochondrial content of germinal epithelium, tubular differentiation (TDI), and spermiogenesis (SPI) indices was analyzed. Finally, the apoptosis was assessed by using TUNEL staining. Observations revealed that the AFB1 remarkably (P |
| doi_str_mv | 10.1002/tox.22627 |
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For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was dissolved in corn oil and ethanol (95:5, v/v) vehicle. The animals in test group subdivided into three groups, which received the AFB1 at a daily dose of 20 μg/kg body weight, through intraperitoneal (i.p.) route, for 7, 14, and 21 days. The mice in the control group received the vehicle alone for 21 days. The expression of Bcl‐2, Bax, p53, and caspase‐3 at both mRNA and protein levels were analyzed by using reverse transcription PCR (RT‐PCR) and immunohistochemistry, respectively. Moreover, the mitochondrial content of germinal epithelium, tubular differentiation (TDI), and spermiogenesis (SPI) indices was analyzed. Finally, the apoptosis was assessed by using TUNEL staining. Observations revealed that the AFB1 remarkably (P < .05) reduced Bcl‐2 expression at both mRNA and protein levels. Up‐regulated Bax, caspase‐3, and p53 expression were revealed in AFB1‐received animals, which developed time‐dependently. Histological examinations exhibited a significant reduction in TDI and SPI indices. Finally, the AFB1‐induced apoptosis index increased time‐dependently. In conclusion, the AFB1 adversely affects the spermatogenesis via inducing oxidative stress, diminishing cellular mitochondrial content and enhancing pro‐apoptotic Bax, caspase‐3, and p53 expression. All these impairments result in mitochondria‐dependent apoptosis.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.22627</identifier><identifier>PMID: 30126036</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>aflatoxin ; Aflatoxin B1 ; Aflatoxin B1 - toxicity ; Albinism ; Animals ; Apoptosis ; Apoptosis - drug effects ; BAX protein ; Body weight ; Caspase ; Corn oil ; Crosslinking ; DNA ; Epithelium ; Ethanol ; Fuel consumption ; Gene expression ; Immunohistochemistry ; In Situ Nick-End Labeling ; intrinsic apoptosis ; Male ; Mice ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - physiology ; Nucleotide sequence ; Organ Size - drug effects ; Oxidative stress ; Oxidative Stress - drug effects ; p53 Protein ; PCR ; Proteins ; Reverse transcription ; Spermatogenesis ; Spermatogenesis - drug effects ; Spermiogenesis ; Testis - drug effects ; Testis - growth & development ; Testis - metabolism ; Transcription</subject><ispartof>Environmental toxicology, 2018-11, Vol.33 (11), p.1204-1213</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3907-fcbeef9a6d2ac826d8bda57f6fbf2079e8bc75a034cf68b0e5be4db103f9c4a33</citedby><cites>FETCH-LOGICAL-c3907-fcbeef9a6d2ac826d8bda57f6fbf2079e8bc75a034cf68b0e5be4db103f9c4a33</cites><orcidid>0000-0002-4309-4831</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30126036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yasin, Malekzadeh</creatorcontrib><creatorcontrib>Mazdak, Razi</creatorcontrib><creatorcontrib>Mino, Ilkhanipour</creatorcontrib><title>Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria‐dependent apoptosis</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>The present experimental study was carried out to investigate the crosslink between aflatoxin B1 (AFB1)‐induced oxidative stress and mitochondria‐dependent apoptosis in testicles. For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was dissolved in corn oil and ethanol (95:5, v/v) vehicle. The animals in test group subdivided into three groups, which received the AFB1 at a daily dose of 20 μg/kg body weight, through intraperitoneal (i.p.) route, for 7, 14, and 21 days. The mice in the control group received the vehicle alone for 21 days. The expression of Bcl‐2, Bax, p53, and caspase‐3 at both mRNA and protein levels were analyzed by using reverse transcription PCR (RT‐PCR) and immunohistochemistry, respectively. Moreover, the mitochondrial content of germinal epithelium, tubular differentiation (TDI), and spermiogenesis (SPI) indices was analyzed. Finally, the apoptosis was assessed by using TUNEL staining. Observations revealed that the AFB1 remarkably (P < .05) reduced Bcl‐2 expression at both mRNA and protein levels. Up‐regulated Bax, caspase‐3, and p53 expression were revealed in AFB1‐received animals, which developed time‐dependently. Histological examinations exhibited a significant reduction in TDI and SPI indices. Finally, the AFB1‐induced apoptosis index increased time‐dependently. In conclusion, the AFB1 adversely affects the spermatogenesis via inducing oxidative stress, diminishing cellular mitochondrial content and enhancing pro‐apoptotic Bax, caspase‐3, and p53 expression. All these impairments result in mitochondria‐dependent apoptosis.</description><subject>aflatoxin</subject><subject>Aflatoxin B1</subject><subject>Aflatoxin B1 - toxicity</subject><subject>Albinism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>BAX protein</subject><subject>Body weight</subject><subject>Caspase</subject><subject>Corn oil</subject><subject>Crosslinking</subject><subject>DNA</subject><subject>Epithelium</subject><subject>Ethanol</subject><subject>Fuel consumption</subject><subject>Gene expression</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>intrinsic apoptosis</subject><subject>Male</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Nucleotide sequence</subject><subject>Organ Size - drug effects</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>p53 Protein</subject><subject>PCR</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Spermatogenesis</subject><subject>Spermatogenesis - drug effects</subject><subject>Spermiogenesis</subject><subject>Testis - drug effects</subject><subject>Testis - growth & development</subject><subject>Testis - metabolism</subject><subject>Transcription</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kbtuFDEUhi0EIiFQ8ALIEg0Uk_iy4xnTLRGQSJHSBInO8uUYHGbswZ4h2Y42XZ6RJ8HshhSRqGwdff589P8IvaTkkBLCjuZ0fciYYN0jtE9bxpqOdf3j7Z00K9LTPfSslEtCiBSteIr2OKFMEC720c3aD7q-DxG_pziMkw654DJBHuv4K0QoobzD64jhug7DCHHWAy7z4jbYp4xtTqUMIX7HBuYrgIirzOk5_IRKZSgF6-jwGOZkv6XoctC_f906mCC66sJ6StOc6ifP0ROvhwIv7s4D9Pnjh4vjk-bs_NPp8fqssVySrvHWAHiphWPa9ky43jjddl544xnpJPTGdq0mfGW96A2B1sDKGUq4l3alOT9Ab3beKacfC5RZjaFYGAYdIS1FMSIp461ktKKvH6CXacmxbqcYZYR2klNZqbc7ahtFBq-mmpPOG0WJ-tuPqvmqbT-VfXVnXMwI7p78V0gFjnbAVRhg83-Tujj_slP-AYqZn1c</recordid><startdate>201811</startdate><enddate>201811</enddate><creator>Yasin, Malekzadeh</creator><creator>Mazdak, Razi</creator><creator>Mino, Ilkhanipour</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>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4309-4831</orcidid></search><sort><creationdate>201811</creationdate><title>Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria‐dependent apoptosis</title><author>Yasin, Malekzadeh ; Mazdak, Razi ; Mino, Ilkhanipour</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3907-fcbeef9a6d2ac826d8bda57f6fbf2079e8bc75a034cf68b0e5be4db103f9c4a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>aflatoxin</topic><topic>Aflatoxin B1</topic><topic>Aflatoxin B1 - toxicity</topic><topic>Albinism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>BAX protein</topic><topic>Body weight</topic><topic>Caspase</topic><topic>Corn oil</topic><topic>Crosslinking</topic><topic>DNA</topic><topic>Epithelium</topic><topic>Ethanol</topic><topic>Fuel consumption</topic><topic>Gene expression</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>intrinsic apoptosis</topic><topic>Male</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - physiology</topic><topic>Nucleotide sequence</topic><topic>Organ Size - drug effects</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>p53 Protein</topic><topic>PCR</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Spermatogenesis</topic><topic>Spermatogenesis - drug effects</topic><topic>Spermiogenesis</topic><topic>Testis - drug effects</topic><topic>Testis - growth & development</topic><topic>Testis - metabolism</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yasin, Malekzadeh</creatorcontrib><creatorcontrib>Mazdak, Razi</creatorcontrib><creatorcontrib>Mino, Ilkhanipour</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yasin, Malekzadeh</au><au>Mazdak, Razi</au><au>Mino, Ilkhanipour</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria‐dependent apoptosis</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2018-11</date><risdate>2018</risdate><volume>33</volume><issue>11</issue><spage>1204</spage><epage>1213</epage><pages>1204-1213</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract>The present experimental study was carried out to investigate the crosslink between aflatoxin B1 (AFB1)‐induced oxidative stress and mitochondria‐dependent apoptosis in testicles. For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was dissolved in corn oil and ethanol (95:5, v/v) vehicle. The animals in test group subdivided into three groups, which received the AFB1 at a daily dose of 20 μg/kg body weight, through intraperitoneal (i.p.) route, for 7, 14, and 21 days. The mice in the control group received the vehicle alone for 21 days. The expression of Bcl‐2, Bax, p53, and caspase‐3 at both mRNA and protein levels were analyzed by using reverse transcription PCR (RT‐PCR) and immunohistochemistry, respectively. Moreover, the mitochondrial content of germinal epithelium, tubular differentiation (TDI), and spermiogenesis (SPI) indices was analyzed. Finally, the apoptosis was assessed by using TUNEL staining. Observations revealed that the AFB1 remarkably (P < .05) reduced Bcl‐2 expression at both mRNA and protein levels. Up‐regulated Bax, caspase‐3, and p53 expression were revealed in AFB1‐received animals, which developed time‐dependently. Histological examinations exhibited a significant reduction in TDI and SPI indices. Finally, the AFB1‐induced apoptosis index increased time‐dependently. In conclusion, the AFB1 adversely affects the spermatogenesis via inducing oxidative stress, diminishing cellular mitochondrial content and enhancing pro‐apoptotic Bax, caspase‐3, and p53 expression. All these impairments result in mitochondria‐dependent apoptosis.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>30126036</pmid><doi>10.1002/tox.22627</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4309-4831</orcidid></addata></record> |
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| subjects | aflatoxin Aflatoxin B1 Aflatoxin B1 - toxicity Albinism Animals Apoptosis Apoptosis - drug effects BAX protein Body weight Caspase Corn oil Crosslinking DNA Epithelium Ethanol Fuel consumption Gene expression Immunohistochemistry In Situ Nick-End Labeling intrinsic apoptosis Male Mice Mitochondria Mitochondria - drug effects Mitochondria - physiology Nucleotide sequence Organ Size - drug effects Oxidative stress Oxidative Stress - drug effects p53 Protein PCR Proteins Reverse transcription Spermatogenesis Spermatogenesis - drug effects Spermiogenesis Testis - drug effects Testis - growth & development Testis - metabolism Transcription |
| title | Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria‐dependent apoptosis |
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