Please use this identifier to cite or link to this item: http://localhost:80/xmlui/handle/123456789/16404
Title: Potent antioxidative DNA damage of selected Saudi medicinal plants in cultured human lymphocytes
Authors: Haytham Mahmoud Daradka
Omar Flah Khabour
Mohammad Kdaimes Alotaibi
Keywords: DNA damage
8-OHdG
plant extract
cultured lymphocytes
cultured lymphocytes
antioxidants
Issue Date: 10-Jul-2018
Publisher: Karachi: Faculty of Pharmacy & Pharmaceutical Sciences University of Karachi
Citation: Daradka, H. M., Khabour, O. F., & Alotaibi, M. K. (2018). Potent antioxidative DNA damage of selected Saudi medicinal plants in cultured human lymphocytes. Pakistan Journal of Pharmaceutical Sciences, 31.
Abstract: Oxidative stress is a condition that might predispose the individuals to diseases including cancer. The 8- hydroxydeoxyguanosine (8-OHdG) is a marker that reflects oxidative DNA damage in the body. In this study, seven Saudi medicinal plants were investigated for their potential against oxidative DNA damage using the 8-OHdG assay in cultured human lymphocytes. Extracts at 10-100µg/mL from Nigella sativa black seeds, Olea chrysophylla (aerial parts) and Pulicaria crispa (aerial parts) significantly decreased levels of 8-OHdG (P<0.01), suggesting their usefulness as protective agents against oxidative DNA damage. The order of the antioxidative DNA damage effect of the extracts at 100µg/mL was Pulicaria crispa (36%) >Olea chrysophylla (24%) >Nigella sativa (18%). On the other hand, extracts of Bupleurum falcatum L at 100ug/mL induced significant increases in the 8-OHdG biomarker (P<0.01). Finally, Ficus palmate, Zygophyllum Simplex, Citrullus colocynthis did not modulate levels of 8-OHdG in cultured human lymphocytes at examined concentrations (10 and 100µg/mL, P>0.05). In conclusion, extracts from Nigella sativa, Olea chrysophylla and Pulicaria cripa medicinal plants can be used as useful agents to counteract oxidative DNA damage in cultured cells.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/16404
ISSN: 1011-601X
Appears in Collections:Issue No.4 (Supplementary)

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