Browsing by Author "Z. Gad, Mohamed"

Now showing 1 - 5 of 5

Addressing the link between paraoxonase-1 gene variants and the incidence of early onset myocardial infarction
(2015) F. Abdel Rahman, Mohamed; M. Hashad, Ingy; Abou-Aisha, Khaled; M. Abdel-Maksoud, Sahar; Z. Gad, Mohamed
The enzyme paraoxonase-1 (PON1) represents an endogenous defense mechanism against vascular oxidative stress, thereby contributing to the prevention of atherosclerosis. Several polymorphisms have been reported in the PON1 gene, including Q192R. PON1 phenotype is commonly expressed as the paraoxonase/arylesterase ratio (PON/ARE). The major aim of this study was
C242T polymorphism of NADPH oxidase p22phox gene reduces the risk of coronary artery disease in a random sample of Egyptian population
(Springer Netherlands, 2014) M. Hashad, Ingy; F. Abdel Rahman, Mohamed; M. Abdel-Maksoud, Sahar; S. Amr, Khalda; K. Effat, Laila; M. Shaban, Gamal; Z. Gad, Mohamed
The p22phox protein subunit is essential for NADPH oxidase activity. The prevalence of C242T variants of p22phox gene was studied in 101 healthy Egyptian controls and 104 acute myocardial infarction (AMI) Egyptian patients. Contribution of oxidative stress, represented by serum oxidized-LDL (ox-LDL), in development of AMI was also examined and correlated with C242T gene variants. Genotyping and ox-LDL were assessed by PCR–RFLP and ELISA. Results showed that wild type CC genotype is prevalent in 27 % of controls; CT and TT are in 72 and 1 %. In patients, the distribution was 40.2, 59.8 and 0 % for CC, CT and TT; respectively, showing a significant difference (p = 0.0259). Serum ox-LDL levels were higher in patients than controls (p ≤ 0.0001). Subjects having CT genotype had lower levels of ox-LDL than CC genotype (p ≤ 0.005). C242T polymorphism of p22phox gene of NADPH oxidase is a novel genetic marker associated with reduced susceptibility to AMI.
Endothelial nitric oxide synthase (G894T) gene polymorphism in a random sample of the Egyptian population: comparison with myocardial infarction patients
(Mary Ann Liebert, Inc., 2012) Z. Gad, Mohamed; F. Abdel Rahman, Mohamed; Abou-Aisha, Khaled; M. Hashad, Ingy; M. Abdel-Maksoud, Sahar; M. Farag, Nabil
im: The aim of this study was to detect endothelial nitric oxide synthase (eNOS) Glu298Asp gene variants in a random sample of the Egyptian population, compare it with those from other populations, and attempt to correlate these variants with serum levels of nitric oxide (NO). The association of eNOS genotypes or serum NO levels with the incidence of acute myocardial infarction (AMI) was also examined. Methods: One hundred one unrelated healthy subjects and 104 unrelated AMI patients were recruited randomly from the 57357 Hospital and intensive care units of El Demerdash Hospital and National Heart Institute, Cairo, Egypt. eNOS genotypes were determined by polymerase chain reaction–restriction fragment length polymorphism. Serum NO was determined spectrophotometrically. Results: The genotype distribution of eNOS Glu298Asp polymorphism determined for our sample was 58.42% GG (wild type), 33.66% GT, and 7.92% TT genotypes while allele frequencies were 75.25% and 24.75% for G and T alleles, respectively. No significant association between serum NO and specific eNOS genotype could be detected. No significant correlation between eNOS genotype distribution or allele frequencies and the incidence of AMI was observed. Conclusion: The present study demonstrated the predominance of the homozygous genotype GG over the heterozygous GT and homozygous TT in random samples of Egyptian population. It also showed the lack of association between eNOS genotypes and mean serum levels of NO, as well as the incidence of AMI.
Exploring genetic susceptibility to cardiovascular disease in Egyptians: Correlation to biochemical investigations
(SPANDIDOS PUBL LTD, 2013) Z. Gad, Mohamed; I. Hassanein, Sally; F. Abdel Rahman, Mohamed; M. Hashad, Ingy; M. Abdel-Maksoud, Sahar; Abou-Aisha, Khaled
Nitric Oxide Regulating Proteins as Biochemical and Genetic Markers of Coronary Artery Disease
(Springer Netherlands, 2016) Z. Gad, Mohamed; M. Abdel-Maksoud, Sahar; I. Hassanein, Sally; M. Hashad, Ingy; F. Abdel Rahman, Mohamed; A. Abu el Maaty, Mohamed; M. Shaban, Gamal; Abou-Aisha, Khaled
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Despite huge efforts and great advances in studying the genetic component of CVD, there is still a great need for exploring the genetic and environmental factors contributing to the development of this disease. Among these factors evolve modulation of nitric oxide (NO) homeostasis and oxidative stress as central players according to recent reports. A wide range of biochemical disturbances, including reduced bioavailability of NO and oxidative stress, has been shown to be associated with endothelial dysfunction (ED). Many studies described the contribution of ED in the predisposition of CVD, particularly coronary artery disease (CAD). Recent evidence indicates that ED may be genetically determined. This chapter points out to the key players that influence vascular NO levels and their role in the protection against and/or predisposition to CAD