Abstract
The purpose of this study was to investigate the synergistic effects of calcium ion-protein energy malnutrition (Ca2+-PEM) and methanolic extract of Plumbago zeylanica (Pz) root on mitochondria permeability transition pore (MPTP). Twenty-four male Wistar rats were studied. The Wistar rats were divided into two groups (experimental and control) of 12 each. The experimental rats were fed with protein-deficient diet, and the control rats were fed with normal rat chow and water ad libitum for 42 days. To monitor MPTP induction and inhibition in both experimental and control Wistar rats, 3 mM Ca2+, 1 mM Mg2+, 120, 160, and 200 μg/ml of Pz extract were used. The rats were sacrificed, and mitochondria were isolated from the livers to monitor MPTP. Our study showed that Ca2+ and Mg2+ induced and inhibited MPTP, respectively. However, PEM drastically increased Ca2+ and Mg2+ MPTP induction and inhibition, respectively, when compared to control. At varying dose and timing, Pz extracts steadily induce MPTP in both experimental and control Wistar rats. Taken together, the results suggest that Ca2+-PEM increased the MPTP induction, while PEM decreased the MPTP induction of Pz extract in dose- and time-dependent pattern when compared to the control that plausibly suggests that PEM may increase Ca2+ induction of MPTP as well mitigate therapeutic effects of Pz extract in diseases related to mitochondria targeting.
Highlights
Mitochondria are unique organelles because their structures provide compartmentalization of metabolism and are helpful in the maintenance of electron gradient across the membrane that allows generation of adenosine triphosphate (ATP), which is essential for life sustenance [1,2,3]
The role of mitochondria in cell death, in this case, involves the mechanisms adopted by the organelle within cells via induction of mitochondria permeability transition pore (MPTP)
We investigated the synergistic effects of Ca2 -Protein-energy malnutrition (PEM) and methanolic extract of Plumbago zeylanica (Pz) root on MPTP in Wistar rats
Summary
Mitochondria are unique organelles because their structures provide compartmentalization of metabolism and are helpful in the maintenance of electron gradient across the membrane that allows generation of adenosine triphosphate (ATP), which is essential for life sustenance [1,2,3]. It becomes imperative to regulate intracellular Ca2 concentration and RORs generated via mitochondria because of its functional role in mediating several cellular activities such as signaling, proliferation, and cell death [4,5,6]. The role of mitochondria in cell death, in this case, involves the mechanisms adopted by the organelle within cells via induction of mitochondria permeability transition pore (MPTP). MPTP induction is characterized as a major event that precedes cell death. These events involved the activity of noxious stimuli such as Ca2 overload, oxidative stress caused by ROR, and several proapoptotic proteins (BCL-2 family) in the inner membrane of the mitochondria [7,8,9,10]. BCL-2 family is localized in endoplasmic reticulum (ER) membranes where they regulate intracellular Ca2 homeostasis in ER [10,11,12,13]
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