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ORIGINAL ARTICLE
Year : 2015  |  Volume : 7  |  Issue : 5  |  Page : 63-68

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


1 Department of Biological Sciences, Covenant University, Ota, Nigeria
2 Department of Biochemistry, University of Ibadan, Iba, Nigeria
3 Department of Biochemistry, University of Ibadan, Iba; Department of Biological Sciences, Crawford University, Igbesa, Nigeria

Correspondence Address:
Oluwatobi Samuel Adegbite
Department of Biological Sciences, Covenant University, Ota
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-8490.157998

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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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