scholarly journals The antioxidant paradox: Damage and defence

2006 ◽  
Vol 28 (5) ◽  
pp. 9-12
Author(s):  
David A. Bender
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vitamin E ◽  
Epidemiological Studies ◽  
Plasma Lipoproteins ◽  
Radical Chain ◽  
Chain Reactions ◽  
Key Factor ◽  
Intervention Trials ◽  
Radical Damage

Over the last three decades, a considerable body of evidence has accumulated to suggest that a key factor in the development of both cancer and coronary heart disease is damage to tissues or plasma lipoproteins caused by free radicals. The majority of radicals that damage tissues are reactive oxygen species, and compounds that can quench potentially damaging radical chain reactions are therefore generally referred to as antioxidants. Epidemiological studies have shown a negative correlation between intakes of antioxidants (especially vitamin E and -carotene) and the incidence of cancer and coronary heart disease, and a positive correlation between markers of radical damage and disease. At the molecular level, there are sound theories to explain how radical damage can lead to cancer and coronary heart disease, and how antioxidants may provide protection. However, the results of intervention trials of vitamin E and -carotene have been, at best, disappointing; indeed, many trials have shown increased death among people taking supposedly protective antioxidant supplements. This is the antioxidant paradox.

scholarly journals The abnormal regulation of spliceosome may be a key factor for coronary heart disease: a simple bioinformatics analysis

2020 ◽  
Author(s):  
Zhaoshui Li ◽  
Wei Sheng ◽  
Yifan Chi
Keyword(s):  
Gene Expression ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gene Expression Omnibus ◽  
Network Control ◽  
Biological Database ◽  
Bioinformatics Analyses ◽  
Chain Reactions ◽  
Go Annotation ◽  
Key Factor

Abstract Background: Cardiovascular Diseases (CVDs) has become a major disease threatening human health. As the main species of CVDs, coronary heart disease (CHD) is becoming more and more common. The pathogenesis of CHD, especially at the molecular level, is not entirely clear up to now. Explaining the pathogenesis of CHD is particularly important for its treatment and prognosis. Biological database data analysis via bioinformatics has been an important method for studying gene expression strategy in multiple human disease. The aim of this study was to identify key different expressed genes (DEGs) in CHD and elucidate the biological process of it.Methods: A total of two published microarray datasets of CHD was downloaded from the Gene Expression Omnibus (GEO). Then, bioinformatics analyses including differentially expressed genes (DEGs) analysis, venn analysis, gene ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein and protein interaction (PPI) network construction was performed. Quantitative real-time polymerase chain reactions (RT-qPCR) were used to detect the expression levels of DEGs in CHD.Results: A total of 122 dysregulated genes were selected as DEGs in CHD. The GO annotation analysis displayed these DEGs involved in DNA transcription and mRNA splicing regulation. The DEGs regulatory network showed the downregulated genes LUC7L3, HNRNPA1, SF3B1, ARGLU1, SRSF5, SRSF11, SREK1, PNISR, DIDO1, ZRSR2 and NKTR were located in the network control center, which were the spliceosome related genes. The RT-qPCR results were consistent with our microarray analysis.Conclusion: The abnormal regulation of spliceosome might be a key factor in the development of CHD, which must play key roles in cardiovascular disease (CVD), especially in CHD. Our study has provided a new idea for the treatment and prognosis of CHD, and the spliceosome might be the potential prognostic biomarkers of it.

scholarly journals Coronary heart disease: dietary links and pathogenesis

2001 ◽  
Vol 4 (2b) ◽  
pp. 459-474 ◽  
Author(s):  
Serge Renaud ◽  
Dominique Lanzmann-Petithory
Keyword(s):  
Fatty Acids ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Saturated Fatty Acids ◽  
Epidemiologic Studies ◽  
Key Factors ◽  
Alpha Linolenic Acid ◽  
Intervention Trials ◽  
The Relationship

AbstractFor decades it has been postulated that the main environmental factor for coronary heart disease (CHD) was the intake of saturated fatty acids (SFA). Nevertheless, confirmation of the role of SFA in CHD through intervention trials has been disappointing. It was only when the diet was enriched in n-3 fatty acids that CHD was significantly prevented, especially cardiac death.In addition to n-3 fatty acids, many other foodstuffs or nutrients such as fibers, antioxidants, folic acid, calcium and even alcohol contribute to prevent CHD. Thus the relationship between diet and CHD morbidity and mortality appears to be much more complex than formerly suspected considering as key factors only SFA, linoleic acid, cholesterol and atherosclerosis. Some of the mechanisms are briefly described, but many additional nutrients (or non nutrients) may also play an important role in the pathogenesis of CHD.Finally, as a result of the most recent epidemiologic studies the ideal diet may comprise: 8% energy from SFA, 5% from polyunsaturated fatty acids with a ratio 5/1 of linoleic/alpha-linolenic acid+longer chains n-3, oleic acid as desired, large intake of cereals, vegetables, legumes and fruits, fish twice a week, cheese and yogurt as dairy products, rapeseed and olive oils as edible fat. Without side effects, such a diet can be highly palatable, easily enjoyed by many populations and may prevent effectively and rapidly (within a few weeks or months) CHD.

Vitamin E Supplements and Coronary Heart Disease

2009 ◽  
Vol 51 (11) ◽  
pp. 333-336 ◽  
Author(s):  
Tim Byers ◽  
Barbara Bowman
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vitamin E

Coffee consumption and risk of type 2 diabetes, cardiovascular diseases, and cancer

2008 ◽  
Vol 33 (6) ◽  
pp. 1269-1283 ◽  
Author(s):  
Rob M. van Dam
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cardiovascular Diseases ◽  
Experimental Studies ◽  
Coffee Consumption ◽  
Density Lipoprotein ◽  
Epidemiological Studies ◽  
Coffee Intake

Numerous epidemiological studies have evaluated the association between coffee consumption and risk of type 2 diabetes, coronary heart disease, and various cancers. This paper briefly reviews the evidence for a relation between coffee consumption and these conditions, with particular attention to methodological issues. Several early studies suggested that coffee consumption could result in a marked increase in risk of coronary heart disease and several types of cancer. However, more recent prospective cohort studies that are less prone to selection and information bias have not confirmed these findings. High consumption of unfiltered types of coffee, such as French press and boiled coffee, has been shown to increase low-density-lipoprotein-cholesterol concentrations. In addition, limiting caffeinated coffee intake during pregnancy seems a prudent choice. However, evidence has been accumulating that frequent consumption of coffee may reduce risk of type 2 diabetes and liver cancer. Further experimental studies are warranted to elucidate the underlying mechanisms and possibly identify the components in coffee that are responsible for these putative effects. In sum, the currently available evidence on coffee and risk of cardiovascular diseases and cancer is largely reassuring, and suggests that, for the general population, addressing other health-related behaviors has priority for the prevention of chronic diseases.

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