Background Cardiovascular diseases are the leading cause of death worldwide, with several conditions being affected by oxidative stress. Ferroptosis, recently identified programmed cell death mechanism, is relies on oxidative stress. This study aimed to determine the expressions of the genes involved in the molecular pathways of oxidative stress and ferroptosis and the association of these genes with CAD risk factors in CAD and non-CAD individuals. Methods and results The blood samples of individuals who underwent coronary angiography were collected and divided according to CAD status. Total RNA isolation was performed using the PAXgene RNA isolation kit from the whole blood samples. The mRNA expression levels of RTN3, GPX4, CAT, HMOX1, ELOVL5, SLC25A1, SLC7A11, and ACSL4 genes were determined using Real-Time PCR. Biochemical analyses were done before coronary angiography, and the results were evaluated statistically. The expression levels of the CAT gene are significantly lower in the CAD group when compared to non-CAD. HMOX1 expression levels are positively correlated with stenosis percentage, Gensini, and SYNTAX scores in the CAD group. RTN3, SLC25A1, and GPX4 mRNA expressions are correlated with HDL-C levels. Moreover, HbA1c levels and BMI, correlate negatively with ACSL4 expression in non-CAD controls. Also, ELOVL5 expression is negatively correlated with total bilirubin and direct bilirubin levels in the CAD group. Conclusions In this study, the genes related to oxidative stress and ferroptosis were found associated with biochemical parameters associated with CAD risk. These preliminary results may provide a new perspective to further studies investigating the reasons behind the identified associations.

Objective: The etiology of Alzheimer's disease (AD) is affected via oxidative stress. Antioxidant enzymes are extremely important in preventing reactive oxygen species (ROS) causing damage in the cell. The changes in expression levels of oxidant and antioxidant genes are key factors in cell response to oxidative stress. As a result, this study investigated the change in expression levels of specific oxidative stress related genes (solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), catalase (CAT) and acylcoa synthetase long chain family member 4 (ACSL4)) in peripheral blood of AD patients. Materials and Methods: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to assess the expression levels of oxidative stress-related genes in 25 AD patients and 22 controls, and the findings were statistically evaluated. Results: SLC7A11, GPX4, CAT, and ACSL4 gene expression levels did not vary significantly between AD patients and controls. The results also showed significant negative correlation between age of onset and ACSL4 expression. Conclusion: This is the first study that evaluated mRNA expression levels of SLC7A11, GPX4 and ACSL4 genes in AD. The results suggested that the peripheral blood expression of above-mentioned genes did not alter in AD. However, due to the small number of subjects, this findings are preliminary and should be validated with a larger number of subjects.

Objective: Inflammation and associated microRNAs (miRNA) both play essential roles in the pathogenesis of Alzheimer’s disease (AD). The expression profile of miRNA’s in an AD brain, also reflected in the peripheral blood mononuclear cells, may give support to the inflammatory changes seen in the course of AD. We aimed to investigate the expression levels of specific inflammatory miRNAs (mir-146a, mir-144, mir-34a) in both blood leukocytes and plasma of AD patients and to evaluate their potential usability as biomarkers in AD diagnosis and to also demonstrate whether the expression of these miRNAs differ between early and late-onset AD patients. Methods: We investigated the expression levels of miRNAs in 16 early-onset and 26 late-onset AD patients and in their respective controls by using qRT-PCR. Results: Plasma mir-144 levels were significantly different between EOAD and LOAD patients (p=0.015). In addition, levels of leukocyte mir-34a were significantly down-regulated in EOAD compared to LOAD patients (p=0.027). Our results also showed significant positive correlations between age and plasma mir144 and leukocyte mir-34a expressions. Conclusion: The differential expression of plasma mir-144 and leukocyte mir-34a between EOAD and LOAD patients might reflect age-dependent changes in miRNA expression and might be independent of the disease status.