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种子油可预防双酚A诱导的睾丸线粒体损伤。

seed oil protects against Bisphenol A-induced testicular mitochondrial damages.

作者信息

Aja Patrick Maduabuchi, Ogwoni Hilary Akobi, Agu Peter Chinedu, Ekpono Ejike Ugbala, Awoke Joshua Nonso, Ukachi Oliver Ugochukwu, Orji Obasi Uche, Ale Boniface Anthony, Nweke Chinonso Peter, Igwenyi Ikechukwu Okorie, Alum Esther Ugo, Chukwu Darlington C, Offor Christian E, Asuk Atamgba Agbor, Eze Ejike Daniel, Yakubu Ojochenemi E, Akobi J B, Ani Onyedika Gabriel, Awuchi Chinaza Godswill

机构信息

Department of Biochemistry Ebonyi State University Abakaliki Nigeria.

Department of Biochemistry Kampala International University Bushenyi Uganda.

出版信息

Food Sci Nutr. 2023 Feb 7;11(6):2631-2641. doi: 10.1002/fsn3.3260. eCollection 2023 Jun.

DOI:10.1002/fsn3.3260
PMID:37324897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10261808/
Abstract

There has been increasing search for the ameliorative properties of seed oils against toxicants. bisphenol A acts as an estrogenic endocrine-disrupting chemical capable of causing male infertility. This study aimed to explore seed oil effects against mitochondrial damage in rats using bisphenol A. Forty-eight rats were randomly assigned to six groups ( = 6) of eight rats each and fed the same food and water for 6 weeks. The group A rats were given 1 mL olive oil, while the ones in group B were given bisphenol A at 100 mL/kg body weight via oral route. Group C received seed oil 7.5 mL/kg body weight seed oil, while group D, group E, and group F were pre-administered bisphenol A at 100 mL/kg body weight, followed by treatment with seed oil at 7.5, 5, and 2.5 mL/kg body weight, respectively. Antioxidant enzymes, glutathione, reactive oxygen species, testicular volume, malondialdehyde, body weight, and testicular studies were done using standard methods. The results of the bisphenol A-administered group showed a significant decrease in the antioxidant enzymes, glutathione, body weight, and testicular volume with elevation in the levels of reactive oxygen species, malondialdehyde, and testicular indices. BPA + CMSO-treated group showed a significant increase in GPx activity compared with BPA-exposed rats. CMSO treatment significantly increased catalase activity in comparison with that of rats exposed to BPA. Remarkably, seed oil and bisphenol A co-administration significantly reversed the abnormalities observed in the dysregulated biochemical biomarkers. Our findings suggest that seed oil has considerable antioxidant potential which can be explored in therapeutic development against systemic toxicity induced by exposure to bisphenol A. seed oil protects against bisphenol A-induced testicular mitochondria damages.

摘要

人们越来越多地探索种子油对有毒物质的改善特性。双酚A是一种具有雌激素活性的内分泌干扰化学物质,能够导致男性不育。本研究旨在探讨种子油对双酚A诱导的大鼠线粒体损伤的影响。48只大鼠被随机分为6组(每组8只),并给予相同的食物和水,持续6周。A组大鼠给予1毫升橄榄油,而B组大鼠通过口服途径给予100毫克/千克体重的双酚A。C组大鼠接受7.5毫升/千克体重的种子油,而D组、E组和F组大鼠先给予100毫克/千克体重的双酚A,随后分别给予7.5、5和2.5毫升/千克体重的种子油进行治疗。使用标准方法进行抗氧化酶、谷胱甘肽、活性氧、睾丸体积、丙二醛、体重和睾丸研究。给予双酚A组的结果显示,抗氧化酶、谷胱甘肽、体重和睾丸体积显著降低,活性氧、丙二醛和睾丸指数水平升高。与暴露于双酚A的大鼠相比,双酚A + CMSO治疗组的GPx活性显著增加。与暴露于双酚A的大鼠相比

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/b559e5f92946/FSN3-11-2631-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/10519b6b8909/FSN3-11-2631-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/5f79fb4fe02c/FSN3-11-2631-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/cdcad6e604cc/FSN3-11-2631-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/d6759300bd78/FSN3-11-2631-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/c66027323921/FSN3-11-2631-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/bca179be9e80/FSN3-11-2631-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/bb048fbe7b7f/FSN3-11-2631-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/446d74f98a52/FSN3-11-2631-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/b559e5f92946/FSN3-11-2631-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/10519b6b8909/FSN3-11-2631-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/5f79fb4fe02c/FSN3-11-2631-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/cdcad6e604cc/FSN3-11-2631-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/d6759300bd78/FSN3-11-2631-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/c66027323921/FSN3-11-2631-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/bca179be9e80/FSN3-11-2631-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/bb048fbe7b7f/FSN3-11-2631-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/446d74f98a52/FSN3-11-2631-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c96e/10261808/b559e5f92946/FSN3-11-2631-g009.jpg

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