RESUMEN
BACKGROUND: Cardiovascular diseases are one of the prime causes of mortality globally. Therefore, concerted efforts are made to prevent or manage disruptions from normal functioning of the cardiovascular system. Disruption in lipid metabolism is a major contributor to cardiovascular dysfunction. This review examines how lecithin impacts lipid metabolism and cardiovascular health. It emphasizes lecithin's ability to reduce excess low-density lipoproteins (LDL) while specifically promoting the synthesis of high-density lipoprotein (HDL) particles, thus contributing to clearer understanding of its role in cardiovascular well-being. Emphasizing the importance of lecithin cholesterol acyltransferase (LCAT) in the reverse cholesterol transport (RCT) process, the article delves into its contribution in removing surplus cholesterol from cells. This review aims to clarify existing literature on lipid metabolism, providing insights for targeted strategies in the prevention and management of atherosclerotic cardiovascular disease (ASCVD). This review summarizes the potential of lecithin in cardiovascular health and the role of LCAT in cholesterol metabolism modulation, based on articles from 2000 to 2023 sourced from databases like MEDLINE, PubMed and the Scientific Electronic Library Online. MAIN BODY: While studies suggest a positive correlation between increased LCAT activities, reduced LDL particle size and elevated serum levels of triglyceride-rich lipoprotein (TRL) markers in individuals at risk of ASCVD, the review acknowledges existing controversies. The precise nature of LCAT's potential adverse effects remains uncertain, with varying reports in the literature. Notably, gastrointestinal symptoms such as diarrhea and nausea have been sporadically documented. CONCLUSIONS: The review calls for a comprehensive investigation into the complexities of LCAT's impact on cardiovascular health, recognizing the need for a nuanced understanding of its potential drawbacks. Despite indications of potential benefits, conflicting findings warrant further research to clarify LCAT's role in atherosclerosis.
RESUMEN
Respiratory health in the general population declines regardless of the presence of pulmonary diseases. Oxidative stress has been implicated as one of the mechanisms involved in respiratory dysfunction. This review was to evaluate studies that relate oxidative stress factors with pulmonary function among the general population without prior respiratory illnesses. The search yielded 54 citations. Twenty-one studies qualified for incorporation in this review. Owing to the heterogeneity of the review, studies were discussed based on identified oxidative stress factors responsible for pulmonary dysfunction. Oxidative stress biomarkers, including gene polymorphisms of nuclear factor erythroid 2-related factor 2, heme oxygenase 1, glutathione S transferase, superoxide dismutase, and lipid peroxidation products were involved in lung function decline. In addition, the antioxidant status of individuals in reference to dietary antioxidant intake and exposure to environmental pollutants affected oxidative stress and pulmonary function, as indicated by forced expired volume in one second, forced vital capacity, and forced expiratory flow at 25%-75%. This review indicated that oxidative stress is implicated in the gradual decline of lung function among the general population, and gene polymorphism along the antioxidant defense line and/or their interaction with air pollutants reduce lung function. Different polymorphic forms among individuals explain why the rate of lung function decline differs among people. Dietary antioxidants have respiratory health benefits in antioxidant gene polymorphic forms. Therefore, the genetic composition of an individual may be considered for monitoring and identifying people at risk of respiratory illnesses.