ArticleHeart Asia2011
Smoking is associated with reduced serum paraoxonase, antioxidants and increased oxidative stress in normolipidaemic acute myocardial infarct patients.
Article in Heart Asia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- Deciphering the potential molecular network underlying nicotine- and its metabolite cotinine-induced myocardial infarction via network toxicology, molecular dynamics, and in vitro experimental validation.Functional & integrative genomics · 2026Article
- Observational
- Oxidative Stress Function in Women over 40 Years of Age, Considering Their Lifestyle.Frontiers in endocrinology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParaoxonase is a high-density lipoprotein (HDL)-associated enzyme that protects lipoproteins from oxidative modifications and from becoming atherogenic in nature. Smoking is a well-known major cardiovascular risk factor that promotes lipid peroxidation (LP). The present study examined the hypothesis that smoking modulates the activity of paraoxonase and depletes antioxidants.
aimThe present study evaluated paraoxonase activity, antioxidant status and LP in smoking and non-smoking normolipidaemic acute myocardial infarct (AMI) patients, and results were compared with controls. SETTINGS AND
designThe serum paraoxonase activities, antioxidants and LP were determined in 86 normolipidaemic patients diagnosed of AMI, and 86 age-sex-matched healthy volunteers served as control. MATERIAL AND
methodsSerum paraoxonase activities were measured by enzymatic kit. The glutathione peroxidase, superoxide dismutase and catalase activity was determined by standard methods. Malondialdehyde was measured by the thiobarbituric acid reaction, and conjugated diene levels by the Recknagel and Glende method. Serum uric acid, total bilirubin, serum albumin and lipid profiles were analysed by standard methods. STATISTICS: The values were expressed as mean±SD, and data from the patients and control were compared using the Student t test. RESULTS AND
conclusionThe total cholesterol/HDL cholesterol ratio, triglycerides, low-density lipoprotein cholesterol, low-density lipoprotein/HDL cholesterol ratio and triglyceride/HDL cholesterol ratio were significantly higher, and HDL cholesterol significantly lower in smokers compared with non-smoking AMI patients. Superoxide dismutase, glutathione peroxidase and catalase were significantly higher in non-smokers compared with smokers. Serum albumin, uric acid and bilirubin were higher in the control compared with smoking AMI patients. The malondialdehyde and conjugated dienes were significantly higher, and paraoxonase activities were significantly lower in smokers compared with non-smokers.
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