Vol.9 No.1-3:Parotoid gland secretions of the Egyptian toad (Bufo relgularis): In vivo antitumor effect on Ehrlich ascites carcinoma bearing mice

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By: Sabry Ali El-Naggar1*, Mohamed Aboulfotouh Basyony1, Seham Mohamed El-Feki1*, Ramadan Mahmoud Kandyel1

1Zoology Department, Faculty of Science, Tanta University, Egypt

Abstract

Background: Parotoid gland secretions (PGS) contain several bioactive compounds with potential applications for drug development. Objective: This study was conducted to evaluate the in vivo antitumor effect of PGS collected from the Egyptian toad, Bufo relgularis using Ehrlich ascites carcinoma-bearing mice (EAC). Methods: The median lethal dose (LD50) of PGS was determined, then forty CD-1 female mice were divided into 4 groups (n=10) as follows: Group (Gp1) served as a negative control. Gp2-Gp4 had inoculated intraperitoneally (i.p) with 1×106 EAC cells/mouse. Then, Gp2 was left as a positive control (EAC- bearing mice). After 24 hours, Gp3 had injected i.p with Cisplatin (Cis) (2 mg/kg) on day 1 for 7 consecutive days. Gp4 had injected with 1/10 LD50 of PGS (7.85 mg/kg, b.wt) i.p for 7 consecutive days. All groups were sacrificed on day 14 to collect blood samples. The percentages of total body weight (% bwt) change, tumor volume, and total tumor cell counts were determined. Alanine and aspartate transaminases (ALT and AST), antioxidant /oxidant biomarkers (SOD, CAT, and MDA), and histological investigations of liver tissues were evaluated. Results: The results showed that the % b.wt changes were increased in EAC- bearing mice, while the treatment of EAC- bearing mice with PGS decreased its % b.wt changes. The treatment of EAC- bearing mice with PGS decreased the tumor volume and its counts. PGS treatment led to an improvement in AST, ALT, and antioxidant enzyme activities, and ameliorated the histopathological changes in the liver induced by EAC inoculation. Conclusion: We concluded that PGS had a potential anticancer effect against EAC- bearing mice.

Parotoid-gland-secretions-of-the-Egyptian-toad-Bufo-relgularis-In-vivo-antitumor-effect-on-Ehrlich-ascites-carcinoma-bearing-mice

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Vol.9 No.1 – 2:In Silico approach for identification, prediction of AMPD1 gene nsSNPs associated with Myoadenylate Deaminase deficiency

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By: Abrar Mohamed Gamar Mohamed1,2*,Abdelrahman Hamza Abdelmoneim Hamza2,3, Hiba Awadelkareem Osman Fadl4,5, Afra Mohamed Suliman Albkrye6, Hadeel Abdelsamea Mohamed Ahmed7, Hazem Abdo Mohamed Abubaker8 and Sahar Gamal Elbager9,10

1*Faculty of Medicine, Al-Zaiem Al-Azhari University, Khartoum, Sudan. abrar.gamer94@gmail.com

2Clinical Immunology Resident, Sudan Medical Specialization Board, Khartoum, Sudan.

3Faculty of Medicine, Al-Neelain University, Khartoum, Sudan. abduhamza009@gmail.com

4Department of Haematology, Faculty of Medical Laboratory Sciences, Al-Neelain University, Khartoum, Sudan. heba2015@hotmail.com

5Department of Medical Laboratory, Sudanese Medical Research Association, Khartoum, Sudan.

6Department of Molecular Biology and Bioinformatics, Faculty of Veterinary Medicine, Bahri University, Khartoum, Sudan. aframoh2016@bahri.edu.sd

7Department of Biotechnology, Faculty of Science and Technology, Omdurman Islamic University, Khartoum, Sudan. hadeelabdelsamea@gmail.com

8Department of Clinical Medicine, Faculty of Veterinary Medicine, University of Khartoum, Khartoum, Sudan. mr.haziem@hotmail.com

9Department of Haematology, Faculty of Medical Laboratory Sciences, University of Medical Sciences and Technology, Khartoum, Sudan. saharelbagir@gmail.com

10Department of Pathology, South Egypt Cancer Institute, Assiut University, Assiut, Egypt.

Abstract:

Background: Myoadenylate deaminase deficiency is an autosomal recessive metabolic myopathy caused by mutations in the Adenosine monophosphate deaminase 1 gene. Adenosine monophosphate deaminase 1 gene deficiency is one of the most common causes of exercise-induced myopathy. In this study, non-synonymous single nucleotide polymorphism was analyzed for its functional and structural impact which is deleterious to Adenosine monophosphate deaminase 1 protein. Methods: The data on human Adenosine monophosphate deaminase 1gene was retrieved from the NCBI database on 9 JUNE 2021 and then analyzed using different bioinformatics prediction algorithms, namely: SIFT, PolyPhen-2, PROVEAN, SNAP2, PANTHER, SNPs and GO, PMut, and I-Mutant to detect the deleterious nsSNPs and its association with diseases. In addition, a Consurf web server was used to detect the functional SNPs in the conserved region. Chimera, Project Hope, and MutPred2 software were used to visualize and analyze the effect of nsSNPs on the functions and structure of the AMPD1 protein. Finally, both the STRING database and KEGG were used for the prediction of protein-protein interaction.  Results: A total of 6178 SNPs were reported in the human AMPD1 gene. In this study 583 missense nsSNPs were selected for investigation and only 72 nsSNPs were shortlisted and computationally evaluated for their impact on AMPD1 protein. From all servers that were used collectively (K320I, R421W, R458C, R458H, R51C, R757L, R761H, and G246S) nsSNPs were predicted as deleterious, associated with disease, highly conserved, and decrease effective stability of AMPD1 protein. In addition, the AMPD1 protein was predicted to have strong interactions with ten proteins involved in various ranges of biological processes.

Conclusion: The present study undertakes a systematic bioinformatics approach to identify functionally important nsSNPs in the human AMPD1 gene to understand how these mutations affect the protein function and structure and hence promote a myoadenylate deaminase deficiency.

In_Silico_approach_for_identification_prediction_of_AMPD1_gene

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