Influence of Borassus flabellifer Endocarps Hydrolysate on Fungal Biomass and Fatty Acids Production by the Marine Fungus Aspergillus sp.

Polyunsaturated Fatty Acids (PUFAs) are important nutrients for human health. We aimed to evaluate the efficiency of marine water fungus Aspergillus sp. (Accession no: MZ505709) for lipid biosynthesis. The Yeast Extract Glucose (YEG) medium was supplemented with different concentration of Borassus flabellifer Endocarps Hydrolysate (BFEH; 1-5%) to evaluate the fungal biomass and its lipid accumulation. The combination of glucose and BFEH as carbon source increased the fresh weight (25.43 ± 0.33 g/L), dry weight (21.39 ± 0.77 g/L) and lipid yield (3.14 ± 0.09 g/L) of fungal biomass. The lipid content of dried fungal biomass has shown 91.08 ± 5.07 mg cod liver oil equivalents/g and 125.98 ± 5.96 mg groundnut oil equivalents/g biomass. GC-MS and NMR spectrometry analysis revealed the compounds involved in fatty acid metabolism and lipid signaling pathways along with the presence of linolenic acid. Interestingly, fungus grown in BFEH enriched medium has recorded the maximum amount of lipids with major fatty acid derivatives. Increase in the growth rate of Artemia franciscana was observed, when the extracted fungal lipid was supplemented as a food supplement. Therefore, this study suggests that marine fungal lipid may serve as potential natural compound as nutraceuticals and aquafeeds.

Myricetin: versatile plant based flavonoid for cancer treatment by inducing cell cycle arrest and ROS-reliant mitochondria-facilitated apoptosis in A549 lung cancer cells and in silico prediction.

Myricetin is categorized under the secondary metabolite flavonoid which includes a diverse range of consumable plant parts, and it has a potential against several classes of cancer including cancers and tumors. In the present study, the anticancer potential of the unique flavonoid-myricetin in A549 lung cancer cells was evaluated. Among different doses of myricetin, 73 µg/ml was more effective to prevent the cancer cell growth. It also promoted sub-G1 phase aggregation of cells and a equivalent decrease in the fraction of cells entering the S and subsequent phase which indicates apoptotic cell death. Myricetin generated enormous free radicals and, altered the potential of mitochondrial membrane in A549 cells as paralleled to untreated cells. In addition, myricetin treatment intensified the expression of P53 and relegated the expression of EGFR in A549 cells. These results suggested that myricetin exhibits cytotoxic potential by arresting the progression of cell cycle and ROS-dependent mitochondria-mediated mortality in cancer A549 lung cancer cells and it would be useful to develop as a drug candidate for lung cancer therapeutics. In silico experiments were carried out against human EGFR and P53 tumor suppressor protein to gain more insights into the binding mode of the myricetin may act as significant potential for anticancer therapy.