Browsing by Author "Hassan, Amr"

Filter results by typing the first few letters
Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Enhancement of Vitamin C’s Protective Effect against ThimerosalInduced Neurotoxicity in the Cerebral Cortex of Wistar Albino Rats: An In Vivo and Computational Study
    (American Chemical Society, 2024-01) Hassan, Amr; Mohsen, Reham; Rezk, Ahmed; Bangay, Gabrielle; Rijo, Patrícia; Soliman, Mona F. M; Hablas, Mohamed G. A; Swidan, Khalifa AbdulRazik K; Mohammed, Tahseen S; Zoair, Mohammad A; Mohamed, Abir A. Khalil; Abdalrhman, Tamer I; Desoky, Ahmad M. Abdel-aleem; Mohamed, Dalia D; Mohamed, Doaa D; Abd El Maksoud, Ahmed I; Mohamed, Aly F
    Vitamin C was examined to ameliorate the neurotoxicity of thimerosal (THIM) in an animal model (Wistar albino rats). In our work, oxidative and antioxidative biomarkers such as SOD, LPO, and GSH were investigated at various doses of THIM with or without concurrent vitamin C administration. Furthermore, the adverse effects of THIM on hepatic tissue and cerebral cortex morphology were examined in the absence or presence of associated vitamin C administration. Also, we studied the effect of vitamin C on the metallothionein isoforms (MT-1, MT-2, and MT-3) in silico and in vivo using the RT-PCR assay. The results showed that the antioxidant biomarker was reduced as the THIM dose was raised and vice versa. THIM-associated vitamin C reduced the adverse effects of the THIM dose. The computation studies demonstrated that vitamin C has a lower ΔG of −4.9 kcal/mol compared to −4.1 kcal/mol for THIM to bind to the MT-2 protein, which demonstrated that vitamin C has a greater ability to bind with MT-2 than THIM. This is due to multiple hydrogen bonds that exist between vitamin C and MT-2 residues Lys31, Gln23, Cys24, and Cys29, and the sodium ion represents key stabilizing interactions. Hydrogen bonds involve electrostatic interactions between hydrogen atom donors (e.g., hydroxyl groups) and acceptors (e.g., carbonyl oxygens). The distances between heavy atoms are typically 2.5−3.5 Å. H-bonds provide directed, highaffinity interactions to anchor the ligand to the binding site. The five H-bonds formed by vitamin C allow it to form a stable complex with MT, while THIM can form two H-bonds with Gln23 and Cys24. This provides less stabilization in the binding pocket, contributing to the lower affinity compared to vitamin C. The histopathological morphologies in hepatic tissue displayed an expansion in the portal tract and the hepatocytes surrounding the portal tract, including apoptosis, binucleation, and karyomegaly. The histopathological morphologies in the brain tissue revealed a significant decrease in the number of Purkinje cells due to THIM toxicity. Interestingly, THIM toxicity was associated with hemorrhage and astrogliosis. Both intracellular and vasogenic edema appeared as the concentrations of THIM rose. Finally, vitamin C ameliorated the adverse effect on the cerebral cortex in Wistar albino rats.
  • Thumbnail Image
    Item
    ZINC OXIDE NANORODS INDUCED APOPTOSIS IN HUMAN PROSTATIC AND HEPATOCELLULAR CARCINOMA VIA MITOCHONDRIA DYSFUNCTION MEDIATED THOUGH BAX/ BCL-2 WITH P53 ACTIVATION
    (Inventi, 2017-06) Sabatier, Jean–Marc; Bakkar, Ashraf; Shebl, Rania I; Mohamed, Aly Fahmy; Hassan, Amr; Gamal, Omar
    The present study aimed to experimentally synthesis zinc oxide nanorods (ZnO NRs) using albumin as bio-template by a sol-gel method and to characterize the products using UV-Visible, FTIR, XRD, TGA and HRTEM. The crystallinity and morphology of the ZnO NRs were confirmed to have an average diameter of 70 nm and 250 nm length. The formation mechanism depends on the nucleation of Zn+2 in sites of the albumin followed by Zn+2 assembly in the cavity of albumin and finally thermal treatment to form ZnO in rod shape then calcination to final form ZnO NRs form as shown in HRTEM. Cytotoxicity of developed ZnO-NRs was conducted using MTT assay on both HepG2 and PC-3 cells. Data revealed that ZnO-NPs were toxic to both HepG2 and PC-3 cell lines displayed a concentration dependent viability. The flow cytometry illustrated that apoptosis of hepatocellular carcinoma (HepG2) depends on the cell growth arrest at G1/S phase indicated that inhibition Cyclin E (CDK 2) while prostatic carcinoma (PC-3) depends cell growth arrest at G2/M phase indicated that inhibition of Cyclin ACDK1. The apoptotic mechanism was investigated using rt-PCR. The apoptotic mechanism in both cell lines HepG2 and PC-3 was depended on the upregulated of Bax protein and down regulation of Bcl-2 indicated that the mechanism of mitochondrial outer membrane permeability (MOMP) or mitochondria dysfunction was dependent on activation of P53 protein.