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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/14590
Title: The therapeutic and antineoplastic effects of vitamin B17 against the growth of solid-form Ehrlich tumours and the associated changes in oxidative stress, DNA damage, apoptosis and proliferation in mice
Authors: El-Masry, Thanaa A.
Al-Shaalan, Nora H.
Tousson, Ehab
Buabeid, Manal
Alyousef, Anhar M.
Keywords: Ehrlich solid tumour
vitamin B17
cytokines
oxidative stress
DNA damage proliferation and apoptotic markers.
Issue Date: 5-Nov-2019
Publisher: Karachi: Faculty of Pharmacy & Pharmaceutical Sciences, Karachi
Citation: El-Masry, T. A., Al-Shaalan, N. H., Tousson, E., Buabeid, M., & Alyousef, A. M. (2019). The therapeutic and antineoplastic effects of vitamin B17 against the growth of solid-form Ehrlich tumours and the associated changes in oxidative stress, DNA damage, apoptosis and proliferation in mice. Pak. J. Pharm. Sci, 32(6), 2801-2810.
Abstract: Many cancer therapies indirectly activate apoptosis by chemical or physical damage of DNA. This study was performed to evaluate protective potential of vitamin B17 (VitB17) against Ehrlich solid tumor (EST) induced changes in the oxidative stress, DNA damage, apoptosis and proliferation in mice. In the experiment, 60 female CD1 mice were randomly and allocated to the following four equal-sized groups [G1, negative control; G2, positive control (VitB17); G3, untreated EST; G4, EST treated with VitB17 (EST+VitB17)]. The untreated EST group displayed major increases in tumor volume, significant increase in the levels of MDA, H2O2, NO, PCNA, TNF-α, AFP and dsDNA and notable reductions in the catalase, GSH, P53 and SOD activities. By contrast, reduced levels of TNF-α, AFP, MDA, H2O2, NO, PCNA and dsDNA, along with enhanced levels of P53 and the antioxidant indicators catalase, GSH and SOD were observed in the EST+VitB17 group. These results indicate the antineoplastic and antioxidant properties of vitamin B17 with the potential to decrease the oxidative stress associated with ESTs by augmenting the antioxidant defence system.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/14590
ISSN: 1011-601X
Appears in Collections:Issue 6 (Supplementary)

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