Global Advanced Research Journal of Educational Research and Reviews (GARJERR) ISSN: 2315-5132

August 2020, 9(1): pp. 001-008

Copyright © 2020 Global Advanced Research Journals

Full Length Research Paper

Prominent effect of Mefloquine on Murine Schistosomiasis Mansoni Schistosomules with no detectable Hepatocyte P53 protein

Rabab S. Zalat^a, Soad I. Hassan^a, Soheir S. Mahmouda Mona Magdi^b,, Hoda Sabry^a, Nevine Guirguis^a and Wafaa El-komy^a

Parasitology^a and Pathology^b DepartmentsmTheodor Bilharz Research Institute, Imbaba, Giza, Egypt P. O. Box 30

Corresponding Author Email: nevinenessimtadros@gmail.com     

Accepted 11 January, 2020

Abstract

The TP53 gene provides instructions for making a protein called tumor protein p53 (or p53). This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing (proliferating) too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches (binds) directly to DNA. When the DNA in a cell becomes damaged by agents such as toxic chemicals, radiation, or ultraviolet (UV) rays from sunlight, this protein plays a critical role in determining whether the DNA will be repaired or the damaged cell will self-destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. By stopping cells with mutated or damaged DNA from dividing, p53 helps prevent the development of tumors. Because p53 is essential for regulating cell division and preventing tumor formation, it has been nicknamed the "guardian of the genome."This work is a trial to elucidate the effect of the antimalarial Mefloquine on the immature stages of Schistosoma mansoni schistosomules in experimental schistosomiasis mansoni. It is also a way to prove that, inspite of this previous effect, the level of hepatocytes p 53 protein is unchanged. Ninty (90) swiss albino mice were used in the experiment. Animals were divided into nine groups according to the time of drug administration. Group 1: infected control. Group 2: Mefloquine was given 24 hours prior to infection. Group 3: Mefloquine was given one week post infection. Group 4:  Mefloquine was given two weeks post infection. Group 5: Mefloquine was given three weeks post infection. Group 6:  Mefloquine was given four weeks post infection. Group 7:  Mefloquine was given five weeks post infection. Group 8:  Mefloquine was given six weeks post infection. Group 9:  Mefloquine was given seven weeks post infection. Each group included three sub-groups corresponding to the three ascending doses used (200, 300 and 400 mg/kg). All animals were sacrificed nine weeks post infection. This study showed that mefloquine doesn’t induce any hepatic dysplastic or malignant changes. This was indicated by the negative nuclear p53 in the hepatocytes with the highest dose of 400 mg/k gm b wt. Therefore, Mefloquine can be safely used as anti- schistosomal, in addition to its known anti –malarial effect. The higher dose of 400 mg/k gm proved to be the most effective in the experiment. Again, this trial disclosed the anti- morbidity role of the drug, by marked improvement in liver pathology, with concurrent drop in both granuloma diameter and numbers. The improvement was more salient in the higher than in the lower doses.    

Keywords: Mefloquine, schistosomiasis, Schistosoma mansoni, P53, protein