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A recent review on the ethnomedicinal, chemical, pharmacological, and toxicological properties of Alstonia boonei revealed the plant's potential in the treatment and management of a range of diseases. However, most of these pharmacological effects are only traceable to the crude form of the plant extract and not specific natural products. Phytochemical investigation of the methanol fraction of the methanol extract of the stem‐bark of Alstonia boonei led to the isolation and identification of 2‐methyl‐3‐propylbutane‐1,4‐diol. The structures were elucidated by the application of 1D‐, and 2D‐NMR spectroscopic analyses and by comparison with literature data. In this study, the membrane stabilizing activity, mitochondrial membrane permeability transition pore opening, cytochrome c release, mitochondrial ATPase activity, and prevention of mitochondrial lipid peroxidation activity of 2‐methyl‐3‐propylbutane‐1,4‐diol (MPBD) isolated from A. boonei were determined. The results showed that MPBD significantly (p <.05) prevented peroxidation of mitochondrial membrane lipids and hemolysis using both the heat‐induced and hypotonic solution‐induced membrane stabilization assays. On the contrary, the compound caused large amplitude swelling of rat liver mitochondria in the absence of calcium, significant (p <.05) cytochrome c release and enhancement of mitochondrial ATPase activity in vitro. Our findings suggest that MPBD showed characteristic biological properties useful in modulating cell death. [ABSTRACT FROM AUTHOR]

The present study investigated the antioxidant and cyto-/mito-protective roles of Methanol Fraction of Ficus mucoso (MFFM) in iron-induced oxidative damage in Drosophila melanogaster. At first, 10-day survival rates were carried out separately on FeSO4 and MFFM, respectively, after which ameliorative effects of MFFM were investigated on FeSO4-induced toxicity for 5 days using biochemical and behavioral markers. Additionally, mitochondria were isolated from treated D. melanogaster to assess mitochondrial Permeability Transition (mPT) pore opening. The results showed that FeSO4 significantly reduced survival rate, total thiol level and activities of catalase and glutathione-S-transferase in D. melanogaster. In addition, treatment with FeSO4 caused increased generation of H2O2, NO (nitrite/nitrates) and acetylcholinesterase (AChE) activity compared with control (p < 0.05). Conversely, MFFM restored FeSO4-induced inhibition of glutathione-S-transferase and catalase activities, as well as glutathione and total thiol levels. FeSO4-induced elevation of AChE activity as well as H2O2 and NO (nitrites/nitrates) levels were ameliorated by MFFM with improved climbing activity. Interestingly, MFFM prevented FeSO4-induced mitochondrial Permeability Transition (mPT) pore opening, and elevated mitochondrial ATPase activity and mitochondrial lipid peroxides generation in D. melanogaster. Taken together, our results demonstrated that iron impaired anti-stress defence capacity, altered behavioral functions, increased generation of mitochondrial malondialdehyde and activated opening of the mPT pore in D. melanogaster. Conversely, methanol fraction of F. mucoso protected against iron-induced cyto-/mito-toxic effects. F. mucoso possibly contain bioactive agents which might be useful in the management of disorders associated with oxidative stress induced by iron and or related metals. [ABSTRACT FROM AUTHOR]

Early detection and treatment of endometrial hyperplasia (EH) is mandatory for endometrial cancer prevention. Several bioactive agents of plant origin have been shown to elicit their chemotherapeutic effect against tumors and cancer via induction of mitochondrial permeability transition(mPT) pore opening. This research was therefore aimed at evaluating the potential chemopreventive effect of methyl palmitate (MP), on estradiol benzoate(EB)-induced EH, looking at the mitochondrial-mediated pathway and other possible mechanisms of action. Mitochondria were isolated using differential centrifugation. The mPT pore, mitochondrial ATPase (mATPase) activity, lipid peroxidation and cytochrome c release were determined by standard methods using spectrophotometer. Uterine interleukin 1b, MDA levels and SOD, GSH activities, were determined using commercially available kits. The uterine histological and immunohistochemical assessment of estrogen receptor (ERα), IL-1b and caspas-3 were carried out. The fibroblast cell count density was determined using histomorphometry. At all the concentrations of MP used, there was no significant induction of mPT pore opening, neither any enhancement of mATPase activity nor release of cytochrome c when compared to the control. Similar pattern of results were recorded for the in vivo study. However, there was marked increase in the uterine MDA and interleukin 1b levels, with concurrent decrease in SOD and GSH activities, in the EB-treated group, which was significantly reversed by MP co-administration. Endometrial Hyperplasia observed in the EB-treated group was ameliorated by MP co-administration. The immunoexpression of ERα and IL-1b in the EB-treated group was reversed by MP co-administration. This study suggests anti-inflammatory, antioxidant and anti-proliferative potential of MP against EB-induced EH. [ABSTRACT FROM AUTHOR]