El-Ghor, A. A., M. M. Noshy, A. Galal, and H. R. H.Mohamed, "Normalization of nano-sized TiO2-induced clastogenicity, genotoxicity and mutagenicity by chlorophyllin administration in mice brain, liver, and bone marrow cells", Toxicological Science, vol. 142, issue 1, pp. 21-32, 2014.
Salem, N. I. S., M. M. Noshy, and A. A. Said, "Modulatory effect of curcumin against genotoxicity and oxidative stress induced by cisplatin and methotrexate in male mice", Food and Chemical Toxicology , vol. 105, issue 105, pp. 370-376, 2017.
Noshy, M. M., A. Saad-Hussein, E. M. Shahy, H. A. I. D. A. N. M. EL-SHORBAGY, M. M. Taha, and E. A. Abdel-Shafy, "Assessment of anticholinesterase toxicity, oxidative stress and antioxidant status in carbamate and organophosphorus pesticides-exposed agricultural workers", International Journal of Pharmaceutical and Clinical Research, vol. 9, issue 3, pp. 205-209, 2017.
Amal Saad-Husseina, M. Noshy, M. Tahaa, H. El-Shorbagy, E. Shahya, and E. A. Abdel-Shafya, "GSTP1 and XRCC1 polymorphisms and DNA damage in agricultural workers exposed to pesticides ", Mutat Res Gen Tox En , vol. 819, issue 819, pp. 20–25, 2017.
El-Ghor, A. A., M. M. Noshy, and J. I. Eid, "Lead acetate and arsenic trioxide induce instability of microsatellites at three different fragile sites (6q21, 9q32-9q33 and 15p14) within the genome of the rat.", Mutation research, vol. 726, issue 2, pp. 195-9, 2011 Dec 24. Abstract

Human exposure to metals is of increasing concern due to the well-documented toxic and carcinogenic effects of metals and metal compounds, and the rising environmental levels due to industrial processes and pollution. It has been reported that metals can be genotoxic by several modes of action including generation of reactive oxygen species and inhibition of DNA repair. The aim of this study was to evaluate microsatellite instability (MSI) in three microsatellite loci (D6mit3, D9mit2 and D15Mgh1) located within three common fragile sites in the genome of the laboratory rat (6q21, 9q32-9q33 and 15p14) exposed to acute and chronic doses of a metal salt (lead acetate trihydrate) and a metalloid oxide (arsenic trioxide). In the acute and sub-chronic studies with the two compounds, MSI was observed in the three loci as deletions or additions of microsatellite repeats. The percentages of MSI were 36.4% and 42.1% for lead acetate and arsenic trioxide, respectively. Results of the present work indicate that the microsatellites located within fragile sites provide a convenient assay system to detect changes in DNA sequences resulting from exposure to genotoxic agents.

El-Ghor, A. A., M. M. Noshy, H. M. El Ashmaoui, J. I. Eid, and M. S. Hassanane, "Microsatellite instability at three microsatellite loci (D6mit3, D9mit2 and D15Mgh1) located in different common fragile sites of rats exposed to cadmium.", Mutation research, vol. 696, issue 2, pp. 160-6, 2010 Feb. Abstract

Cadmium (Cd) is a non-essential element and is a widespread environmental pollutant. Exposure to cadmium can result in cytotoxic, carcinogenic and mutagenic effects. Mutagenesis is an indicative of genetic instability and can be assayed using microsatellites instability. The aim of the present study is to investigate; based on the rat model, the effects of oral acute (single 8.8mg/kg BW, 1/10 LD(50)) and sub-chronic (2.93mg/kg BW, 1/30 LD(50), for 4 weeks) doses of cadmium chloride on microsatellite instability at D6mit3, D9mit2 and D15Mgh1 loci, which are located in three different common fragile sites (6q21, 9q32-q33 and 15p14, respectively), within rat genome. In the acute study, no microsatellite instability (MSI) was observed in all the three tested loci (D6mit3, D9mit2 and D15Mgh1). In the sub-chronic study, the MSI were observed in the three studied loci and was in the form of deletion of 2-3bp or addition of 3-6bp. These finding may indicate the sensitivity of microsatellite sequences located at the fragile sites and the sensitivity of the simple sequence repeats (SSRs) assay for the detection of small variations in DNA sequence. However, additional chronic toxicological trials are needed in order to assess genotoxic effects of chronic exposure to Cd.

Tohamy, A. A., A. A. El-Ghor, S. M. El-Nahas, and M. M. Noshy, "Beta-glucan inhibits the genotoxicity of cyclophosphamide, adriamycin and cisplatin.", Mutation research, vol. 541, issue 1-2, pp. 45-53, 2003 Nov 10. Abstract

The inhibitory effects of beta-glucan (betaG), one of the biological response modifiers, on the induction of chromosomal aberrations in the bone marrow and spermatogonial cells of mice treated with various anti-neoplastic drugs were investigated. beta-Glucan (100 mg/kg bw, i.p.) pre-treatment reduced the total number of cells with structural chromosomal aberrations scored after the treatment with cyclophosphamide (CP) (2.5 mg/kg bw, i.p.) adriamycin (ADR) (12 mg/kg bw, i.p.) and cis-diamminedichloroplatinum-II (cisplatin) (5 mg/kg bw, i.p.) by about 41.1, 26.9 and 57.7% in bone marrow and 44.4, 55 and 57.1% in spermatogonial cells, respectively. This protective effect of beta-glucan could be attributed to its scavenging ability to trap free-radicals produced during the biotransformation of these anti-neoplastic drugs. Beta-glucan also markedly restored the mitotic activity of bone marrow cells that had been suppressed by the anti-neoplastic drugs. These results indicate that in addition to the known immunopotentiating activity of beta-glucan, it plays a role in reducing genotoxicity induced by anti-neoplastic drugs during cancer chemotherapy.

Noshy, M. M., N. A. Hussien, and A. A. El-Ghor, "Evaluation of the role of the antioxidant silymarin in modulating the in vivo genotoxicity of the antiviral drug ribavirin in mice.", Mutation research, vol. 752, issue 1-2, pp. 14-20, 2013 Apr 15. Abstract

Ribavirin (1-β-d-ribofuranosyl-1,2,4-triazole-3-carboxamide) is a widely used broad-spectrum antiviral drug. Recently, several reports revealed genotoxic effects of ribavirin in vivo and in vitro, which were correlated with the production of reactive oxygen species (ROS). This study aimed to evaluate the genotoxicity of ribavirin and to investigate the role of the natural antioxidant silymarin to modulate this genotoxicity. Male albino mice (age, 8-10 weeks) were injected intraperitoneally (i.p.) with ribavirin at three dose levels (20, 75 and 130 mg/kg bw) either in a single injection (acute treatment) or in multiple injections on five consecutive days (sub-acute treatment). Other comparable groups were treated with silymarin (70 mg/kg bw) 1h before the injection with ribavirin. Mice were sacrificed at different sampling times (24, 48 and 72 h) after the last ribavirin treatment. Micronucleus (MN) and single-strand conformation polymorphism (SSCP) assays were used to assess genotoxic and cytotoxic effects of ribavirin and to evaluate the protective effect of the pre-treatment with silymarin. Our results reveal genotoxic and cytotoxic effects of ribavirin in the MN assay. Pre-treatment with silymarin reduced the toxicity of ribavirin. In the SSCP assay, ribavirin treatment did not induce any mutations in the two selected sites in the D-loop of mitochondrial DNA (mtDNA).