Background: Colorectal cancer (CRC) is a leading cause of cancer-related death. Oxidative DNA damage may contribute to cancer risk and the antioxidant paraoxonase is one endogenous free radical scavenger in the human body which could therefore exert an influeence. Purpose: Aim of this study was to determine the role of serum arylesterase (ARE) and paraoxonase 1(PON1) activities in CRC patients and to find any association between (PON1) Q192R and L55M gene polymorphisms in CRC patients. Also the serum ARE and PON1 activities in CRC patients will be investigated before and after surgery Materials and Methods: This study involved a total of 50 patients with newly diagnosed CRC and 80 healthy controls. PON1 and ARE activities were determined using an enzymatic spectrophotometric method. PON1 Q192R and L55M gene polymorphisms were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) based restriction fragment analysis. The restriction enzyme AlwI was used to examine the Q192R polymorphism and Hsp92II for the L55M polymorphism. Results: Significant differences in the PON1 Q192R polymorphism were found between patients and controls. The Q allele was more frequent in the patient group than in controls, while the R allele was more frequent in the controls. Significant differences were found in the L55M polymorphism. Additionally, there were significant differences in L and M allele frequencies (p=0.001). The serum activities of PON1 and ARE were low in QQ and MM genotype. Conclusions: serum PON1 and ARE activities were significantly lower in CRC patients compared to healthy subjects. The R allele may protect against colorectal cancer.
Breast cancers are potentially life threatening malignancies in women. Current evidence indicates that free radicals and mitochondrial DNA damage play a prominent role in the development of breast cancer. Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species (ROS) in the mitochondria. One of the several metabolic pathways involved in breast carcinogenesis is the human polymorphism in the mitochondria targeting sequence Ala 9 Val of the MnSOD gene. It is hypothesized that the valine to alanine substitution seems to alter transport of the enzyme into the mitochondrion, changing its efficacy in fighting oxidative stress. The present study included 24 females with breast cancer, 27females with benign breast lesion and 23 female healthy controls. Whole blood samples were collected, part on heparin for DNA extraction which was used to assay MnSOD polymorphism by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The other part of blood samples was collected on plain tunes and serum together with breast tissue samples were used for estimation of lipid peroxides (LP), nitric oxide (NO) and total superoxide dismutase (SOD) activity. The results of the study showed significant elevations of serum NO mean levels in breast cancer patients (53.57 ±10.6 µmol/l) compared to both control subjects (25.4 ±8.3 µmol/l) and patients with benign breast lesions (23.6 ±7.8 µmol/l), the latter mean level is not significantly different from that of controls. NO levels in breast cancer tissues (7.3±1.3 pmol /mg protein) were significantly higher compared to both control subjects (1.6 ±0.03 pmol /mg protein) and patients with benign breast lesions (3.3±0.7 pmol/mg protein), Also, the latter mean level is significantly higher compared to that of controls. Serum MDA levels in breast cancer patients (1.58 ±104 µmol/l) were not significantly different compared to both control subjects (0.9 ±0.7 µmol/l) and patients with benign breast lesions (1.07 ±0.62 µmol/l), MDA mean levels in breast cancer tissues (244.2±23.1 pmol /mg protein) were significantly higher compared to both control subjects (77.4 ±8.3 pmole /mg protein) and patients with benign breast lesions (91.2±91.2 pmole /mg protein), , the latter mean level is not significantly different from that of controls. Serum total SOD mean activity of breast cancer patients (145.4 ±24.6 U/l) was significantly lower compared to both control subjects (231.5 ±39.4 U/l) and patients Bull. Egypt. Soc. Physiol. Sci. 33 (2) 2013Ahmed et al. 84with benign breast lesions (211.1 ±37.4 U/l), , the latter mean level is not significantly different from that of controls. Total SOD mean activity in breast cancer tissues (9.3±2.7 U/mg protein) were significantly lower compared to both control subjects (25.5 ±1.1 U/mg protein) and patients with benign breast lesions (23.1±2.3 U/mg protein), , the latter mean activity is not significantly different from that of controls. Ala/Val genotype is the most p...
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