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العنوان
Effect of Ketogenic Diet and/or γ-radiation on Ehrlich Solid Carcinoma in Female Mice \
المؤلف
Awad, Walaa Mohamed Abd Elmoniem.
هيئة الاعداد
باحث / ولاء محمد عبد المنعم عوض
مشرف / نورا محمد عفيفي الشيخ
مشرف / هدى محمد إسماعيل
مشرف / مصطفي عسكر عسكر المتولي
تاريخ النشر
2024.
عدد الصفحات
287 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
Biochemistry, Genetics and Molecular Biology (miscellaneous)
تاريخ الإجازة
1/1/2024
مكان الإجازة
جامعة عين شمس - كلية البنات - الكيمياء الحيوية والتغذية
الفهرس
Only 14 pages are availabe for public view

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Abstract

Background: Cancer remains a significant global health concern, prompting exploration into alternative treatment modalities. The ketogenic diet (KD) has emerged as a potential adjunctive therapy due to its purported antitumor effects. Aim: This study investigates the efficacy of the ketogenic diet in conjunction with radiation therapy for treating Ehrlich Solid Carcinoma (ESC) in female Swiss albino mice. Methods: Ninety female Swiss albino mice were divided into equal six groups and subjected to different dietary and treatment regimens over a five-weeks period. Tumor volume, β- hydroxybutyric acid levels, and blood glucose were monitored to assess tumor progression and ketosis. Upon sacrifice, tumor volume, tumor weight and inhibition rate of tumor growth were measured. Various biological measurements were evaluated as changes in body weight, feed intake and feed efficiency ratio and biochemical markers including carbohydrate metabolism and ketosis, aerobic glycolysis, tumor growth factors, oxidative stress /antioxidative markers, cell cycle analysis, apoptosis
]annexin V stanning[ , tumor suppressor protein p53, immunohistochemical analysis (PCNA) and microscopic examination of muscle and tumor tissues. Results: The combination of the ketogenic diet and radiation therapy exhibited the most significant reduction in tumor volume and weight. It decreased body weight, feed intake and feed efficiency ratio. This combination treatment also led to decreases in markers of aerobic glycolysis, hypoxia-inducible factor 1-α, vascular endothelial growth factor, phosphoinositide 3-kinase, malondialdehyde and proliferating cell nuclear antigen. While increasing pyruvate dehydrogenase, reduced glutathione, the sub G1 phase in the cell cycle, apoptosis
]annexin V stanning[ and tumor suppressor protein P53.