Publications by authors named "Amira Ali El-Fallal"

2 Publications

  • Page 1 of 1

Effect of the taxonomic group of fungi and type of substrate on the antioxidant activity of a solid-state fermentation system.

Int Microbiol 2019 Jun 9;22(2):203-215. Epub 2018 Nov 9.

Department of Botany and Microbiology, Faculty of Science, Damietta University, New Damietta City, 34517, Egypt.

The enzymatic and non-enzymatic antioxidant activities of a solid-state fermentation system (SSFS) employing six basidiomycete and four ascomycete fungi on orange peel have been evaluated. Class comparisons revealed highly significant effect of fungal group on the antioxidant activity. Peroxidase activity appeared only in the basidiomycete fungi (particularly Pleurotus columbinus, Ganoderma resinaceum, and Pleurotus floridanus) whereas catalase activity appeared in the two fungal groups in favor of the ascomycetes (particularly Paecilomyces variotii and Aspergillus fumigatus). Maximal peroxidase and minimal catalase activities were found at moderate phenolic content, with extreme phenolic levels leading to low peroxidase activity but high catalase activity. Production of the non-enzymatic antioxidants (phenolics, flavonoids, reducing power, and DPPH scavenging) was in favor of the ascomycetes, which showed great native ability to synthesize flavonoids and also to release flavonoids from orange peel. The basidiomycete fungi, which have limited native ability to produce phenolics, had high ability to consume orange peel phenolics. By contrast, the ascomycete fungi exhibited great native ability for production of phenolics and low ability to consume exogenous phenolics.
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http://dx.doi.org/10.1007/s10123-018-00040-6DOI Listing
June 2019

The molecular basis of cytotoxicity of α-spinasterol from Ganoderma resinaceum: Induction of apoptosis and overexpression of p53 in breast and ovarian cancer cell lines.

J Cell Biochem 2018 05 25;119(5):3892-3902. Epub 2018 Jan 25.

Center of Excellence for Stem Cells and Regenerative Medicine, Zewail City of Science and Technology, Giza, Egypt.

Despite advances in therapy of breast and ovarian cancers, they still remain among the most imperative causes of cancer death in women. The first can be considered one of the most widespread diseases among females, while the latter is more lethal and needs prompt treatment. Thus, the research field can still benefit from discovery of new compounds that can be of potential use in management of these grave illnesses. We hereby aimed to assess the antitumor activity of the phytosterol α-spinasterol isolated from Ganoderma resinaceum mushroom on human breast cancer cell lines (MCF-7, MDA-MB-231), as well as, on human ovarian cancer cell line (SKOV-3). The anti-tumor activity of α-spinasterol, isolated from the mycelial extract of the Egyptian G. resinaceum, on human breast and ovarian cancer cell lines was evaluated by MTT cell viability assay and AnnexinV/propidium iodide apoptosis assay. The molecular mechanism underlying this effect was assessed by the relative expression of the following markers; tumor suppressor (p53, BRCA1, BRCA2), apoptotic marker (Bax) and cell cycle progression markers (cyclin dependent kinases cdk4/6) using real-time PCR. Cell cycle analysis was performed for the three investigated cancer cell lines to explore the effect on cell cycle progression. Our findings showed that α-spinasterol exhibited a higher antitumor activity on MCF-7 cells relative to SKOV-3 cells, while its lowest antitumor activity was against MDA-MB-231 cells. A significant increase in the expression of p53 and Bax was observed in cells treated with α-spinasterol, while cdk4/6 were significantly down-regulated upon exposure to α-spinasterol. Cell cycle analysis of α-spinasterol treated cells showed a G -G arrest. In conclusion, α-spinasterol isolated from G. resinaceum mushroom exerts a potent inhibitory activity on breast and ovarian cancer cell lines in a time- and dose-dependent manner. This can be reasonified in lights of the compound's ability to increase p53 and Bax expressions, and to lower the expression of cdk4/6.
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http://dx.doi.org/10.1002/jcb.26515DOI Listing
May 2018
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