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Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea

BACKGROUND: The induction of the mitochondrial membrane permeability transition (MMPT) pore has been implicated in the cascade of events involved in apoptosis (programmed cell death). Olax subscorpioidea is traditionally used for the treatment of several diseases and infection. However, its role on...

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Autores principales: Adegbite, Oluwatobi Samuel, Akinsanya, Yetunde Ifeoma, Kukoyi, Ayobami Jahdahunsi, Iyanda-Joel, Wisdom O., Daniel, Oluwatoyin O., Adebayo, Abiodun Humphrey
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466771/
https://www.ncbi.nlm.nih.gov/pubmed/26109790
http://dx.doi.org/10.4103/0974-8490.157998
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author Adegbite, Oluwatobi Samuel
Akinsanya, Yetunde Ifeoma
Kukoyi, Ayobami Jahdahunsi
Iyanda-Joel, Wisdom O.
Daniel, Oluwatoyin O.
Adebayo, Abiodun Humphrey
author_facet Adegbite, Oluwatobi Samuel
Akinsanya, Yetunde Ifeoma
Kukoyi, Ayobami Jahdahunsi
Iyanda-Joel, Wisdom O.
Daniel, Oluwatoyin O.
Adebayo, Abiodun Humphrey
author_sort Adegbite, Oluwatobi Samuel
collection PubMed
description BACKGROUND: The induction of the mitochondrial membrane permeability transition (MMPT) pore has been implicated in the cascade of events involved in apoptosis (programmed cell death). Olax subscorpioidea is traditionally used for the treatment of several diseases and infection. However, its role on MMPT is not yet established. This study was aimed at evaluating the effects of varying concentrations of the methanol leaf extract of O. subscorpioidea (MEOS) on MMPT pore opening, mitochondrial adenosine triphosphatase (ATPase), and mitochondrial lipid peroxidation. MATERIALS AND METHODS: Opening of the pore was spectrophotometrically assayed under succinate-energized conditions. RESULTS: In the absence of triggering agent (calcium), MEOS induced MMPT pore opening by 350, 612, 827, 845% at 36, 60, 86 and 112 μg/ml, respectively. MEOS further induced MMPT pore opening in the presence of a triggering agent by 866, 905, 831, 840, 949% at 12, 36, 60, 86 and 112 μg/ml, respectively. The extract significantly induced mitochondrial membrane lipid peroxidation in all the concentration used. MEOS also significantly increased mitochondrial ATP hydrolysis by mitochondrial ATPase in all concentration of the extract used. CONCLUSION: It may be deduced from this results, that MEOS contains certain bioactive components that may find use in pathological conditions that require an enhanced rate of apoptosis.
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spelling pubmed-44667712015-06-24 Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea Adegbite, Oluwatobi Samuel Akinsanya, Yetunde Ifeoma Kukoyi, Ayobami Jahdahunsi Iyanda-Joel, Wisdom O. Daniel, Oluwatoyin O. Adebayo, Abiodun Humphrey Pharmacognosy Res Original Article BACKGROUND: The induction of the mitochondrial membrane permeability transition (MMPT) pore has been implicated in the cascade of events involved in apoptosis (programmed cell death). Olax subscorpioidea is traditionally used for the treatment of several diseases and infection. However, its role on MMPT is not yet established. This study was aimed at evaluating the effects of varying concentrations of the methanol leaf extract of O. subscorpioidea (MEOS) on MMPT pore opening, mitochondrial adenosine triphosphatase (ATPase), and mitochondrial lipid peroxidation. MATERIALS AND METHODS: Opening of the pore was spectrophotometrically assayed under succinate-energized conditions. RESULTS: In the absence of triggering agent (calcium), MEOS induced MMPT pore opening by 350, 612, 827, 845% at 36, 60, 86 and 112 μg/ml, respectively. MEOS further induced MMPT pore opening in the presence of a triggering agent by 866, 905, 831, 840, 949% at 12, 36, 60, 86 and 112 μg/ml, respectively. The extract significantly induced mitochondrial membrane lipid peroxidation in all the concentration used. MEOS also significantly increased mitochondrial ATP hydrolysis by mitochondrial ATPase in all concentration of the extract used. CONCLUSION: It may be deduced from this results, that MEOS contains certain bioactive components that may find use in pathological conditions that require an enhanced rate of apoptosis. Medknow Publications & Media Pvt Ltd 2015-06 /pmc/articles/PMC4466771/ /pubmed/26109790 http://dx.doi.org/10.4103/0974-8490.157998 Text en Copyright: © Pharmacognosy Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Adegbite, Oluwatobi Samuel
Akinsanya, Yetunde Ifeoma
Kukoyi, Ayobami Jahdahunsi
Iyanda-Joel, Wisdom O.
Daniel, Oluwatoyin O.
Adebayo, Abiodun Humphrey
Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title_full Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title_fullStr Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title_full_unstemmed Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title_short Induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of Olax subscorpioidea
title_sort induction of rat hepatic mitochondrial membrane permeability transition pore opening by leaf extract of olax subscorpioidea
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466771/
https://www.ncbi.nlm.nih.gov/pubmed/26109790
http://dx.doi.org/10.4103/0974-8490.157998
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