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Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats

The present study principally sought to investigate the effect of green tea extract (GTE) supplementation on hepatic mitochondrial DNA (mtDNA) damage in alcohol receiving rats. MtDNA was isolated from hepatic tissues of albino wistar rats after alcohol treatment with and without GTE supplementation....

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Autores principales: Reddyvari, Hymavathi, Govatati, Suresh, Matha, Sumanth Kumar, Korla, Swapna Vahini, Malempati, Sravanthi, Pasupuleti, Sreenivasa Rao, Bhanoori, Manjula, Nallanchakravarthula, Varadacharyulu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349453/
https://www.ncbi.nlm.nih.gov/pubmed/28337346
http://dx.doi.org/10.1016/j.jare.2017.02.002
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author Reddyvari, Hymavathi
Govatati, Suresh
Matha, Sumanth Kumar
Korla, Swapna Vahini
Malempati, Sravanthi
Pasupuleti, Sreenivasa Rao
Bhanoori, Manjula
Nallanchakravarthula, Varadacharyulu
author_facet Reddyvari, Hymavathi
Govatati, Suresh
Matha, Sumanth Kumar
Korla, Swapna Vahini
Malempati, Sravanthi
Pasupuleti, Sreenivasa Rao
Bhanoori, Manjula
Nallanchakravarthula, Varadacharyulu
author_sort Reddyvari, Hymavathi
collection PubMed
description The present study principally sought to investigate the effect of green tea extract (GTE) supplementation on hepatic mitochondrial DNA (mtDNA) damage in alcohol receiving rats. MtDNA was isolated from hepatic tissues of albino wistar rats after alcohol treatment with and without GTE supplementation. Entire displacement loop (D-loop) of mtDNA was screened by PCR-Sanger’s sequencing method. In addition, mtDNA deletions and antioxidant activity were measured in hepatic tissue of all rats. Results showed increased frequency of D-loop mutations in alcoholic rats (ALC). DNA mfold analysis predicted higher free energy for 15507C and 16116C alleles compared to their corresponding wild alleles which represents less stable secondary structures with negative impact on overall mtDNA function. Interestingly, D-loop mutations observed in ALC rats were successfully restored on GTE supplementation. MtDNA deletions were observed in ALC rats, but intact native mtDNA was found in ALC + GTE group suggesting alcohol induced oxidative damage of mtDNA and ameliorative effect of GTE. Furthermore, markedly decreased activities of glutathione peroxidise, superoxide dismutase, catalase and glutathione content were identified in ALC rats; however, GTE supplementation significantly (P < 0.05) restored these levels close to normal. In conclusion, green tea could be used as an effective nutraceutical against alcohol induced mitochondrial DNA damage.
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spelling pubmed-53494532017-03-23 Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats Reddyvari, Hymavathi Govatati, Suresh Matha, Sumanth Kumar Korla, Swapna Vahini Malempati, Sravanthi Pasupuleti, Sreenivasa Rao Bhanoori, Manjula Nallanchakravarthula, Varadacharyulu J Adv Res Original Article The present study principally sought to investigate the effect of green tea extract (GTE) supplementation on hepatic mitochondrial DNA (mtDNA) damage in alcohol receiving rats. MtDNA was isolated from hepatic tissues of albino wistar rats after alcohol treatment with and without GTE supplementation. Entire displacement loop (D-loop) of mtDNA was screened by PCR-Sanger’s sequencing method. In addition, mtDNA deletions and antioxidant activity were measured in hepatic tissue of all rats. Results showed increased frequency of D-loop mutations in alcoholic rats (ALC). DNA mfold analysis predicted higher free energy for 15507C and 16116C alleles compared to their corresponding wild alleles which represents less stable secondary structures with negative impact on overall mtDNA function. Interestingly, D-loop mutations observed in ALC rats were successfully restored on GTE supplementation. MtDNA deletions were observed in ALC rats, but intact native mtDNA was found in ALC + GTE group suggesting alcohol induced oxidative damage of mtDNA and ameliorative effect of GTE. Furthermore, markedly decreased activities of glutathione peroxidise, superoxide dismutase, catalase and glutathione content were identified in ALC rats; however, GTE supplementation significantly (P < 0.05) restored these levels close to normal. In conclusion, green tea could be used as an effective nutraceutical against alcohol induced mitochondrial DNA damage. Elsevier 2017-05 2017-02-24 /pmc/articles/PMC5349453/ /pubmed/28337346 http://dx.doi.org/10.1016/j.jare.2017.02.002 Text en © 2017 Production and hosting by Elsevier B.V. on behalf of Cairo University. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Reddyvari, Hymavathi
Govatati, Suresh
Matha, Sumanth Kumar
Korla, Swapna Vahini
Malempati, Sravanthi
Pasupuleti, Sreenivasa Rao
Bhanoori, Manjula
Nallanchakravarthula, Varadacharyulu
Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title_full Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title_fullStr Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title_full_unstemmed Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title_short Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats
title_sort therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial dna damage in albino wistar rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349453/
https://www.ncbi.nlm.nih.gov/pubmed/28337346
http://dx.doi.org/10.1016/j.jare.2017.02.002
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