In vitro induction of rat liver mitochondrial membrane permeability transition pore opening by solvent extracts of Momordica charantia leaves
Abstract
Alteration of mitochondrial functions such as permeability transition (PT), a process associated with
the uncoupling of oxidative phosphorylation, has been found to play a vital role in the apoptotic process induced by
certain anti-cancer agents. When triggered, PT facilitates the release of mitochondrial apoptogenic proteins which
in turn activate the caspase cascade of apoptosis. Thus, this study investigated the in vitro effects of varying
concentrations (0.2, 0.4, 0.6, 0.8 and 1.0 mg/ml) of different leaf extracts [Crude Water-Soluble Extract (CWSE),
Decoction (DE) and Methanol Extract (ME)] of Momordica charantia (M. charantia), a purported anti-cancer plant of
the family Cucurbitaceae on normal rat liver mitochondria. Opening of mitochondrial membrane permeability
transition pore (MMPTP) was spectrophotometrically assayed under succinate-energized condition. Results
obtained showed concentration-dependent and significant (P<0.05) increases in the extents to which MMPTP
opening was induced by the three extract types when compared with the control group. Inductions caused by CWSE
and DE increased with increasing concentrations while those caused by ME decreased with increasing
concentrations, giving the maximum induction at 1.0 mg/ml (8.1-fold increase) of CWSE and the least induction at
1.0 mg/ml (4.3-fold increase) of ME, respectively. Spermine, a reference inhibitor of MMPTP opening, reversed all
observed openings. These results indicate that the tested leaf extracts of M. charantia are potent (CWSE being the
most potent) MMPTP opening inducers and the pathway by which M. charantia causes apoptosis in cancer cells is
probably mitochondrial-mediated (intrinsic).
the uncoupling of oxidative phosphorylation, has been found to play a vital role in the apoptotic process induced by
certain anti-cancer agents. When triggered, PT facilitates the release of mitochondrial apoptogenic proteins which
in turn activate the caspase cascade of apoptosis. Thus, this study investigated the in vitro effects of varying
concentrations (0.2, 0.4, 0.6, 0.8 and 1.0 mg/ml) of different leaf extracts [Crude Water-Soluble Extract (CWSE),
Decoction (DE) and Methanol Extract (ME)] of Momordica charantia (M. charantia), a purported anti-cancer plant of
the family Cucurbitaceae on normal rat liver mitochondria. Opening of mitochondrial membrane permeability
transition pore (MMPTP) was spectrophotometrically assayed under succinate-energized condition. Results
obtained showed concentration-dependent and significant (P<0.05) increases in the extents to which MMPTP
opening was induced by the three extract types when compared with the control group. Inductions caused by CWSE
and DE increased with increasing concentrations while those caused by ME decreased with increasing
concentrations, giving the maximum induction at 1.0 mg/ml (8.1-fold increase) of CWSE and the least induction at
1.0 mg/ml (4.3-fold increase) of ME, respectively. Spermine, a reference inhibitor of MMPTP opening, reversed all
observed openings. These results indicate that the tested leaf extracts of M. charantia are potent (CWSE being the
most potent) MMPTP opening inducers and the pathway by which M. charantia causes apoptosis in cancer cells is
probably mitochondrial-mediated (intrinsic).
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