serum cotinine, thiocyanate, neuron specific enolase and uric acid levels of cigarette smokers

What is it about?

Cigarette smoke contains harmful chemicals with deleterious health effects leading to oxidative stress and neuronal damage. Nerve tissues require significant amounts of nutrients and oxygen via blood flow, smoking constricts blood vessels making them smaller, resulting in less blood and nutrients being delivered to the peripheral nerves. Normal blood vessels have an inner lining, the endothelium that keeps blood flowing smoothly by producing local Nitric oxide (NO). NO aids the relaxation of smooth muscles in the walls of blood vessels and avert cells from sticking to the walls. A disturbance of this mechanism in cigarette smokers via NO bioavailability reduction, leads to impairments of vascular tone and hemostasis and endothelial dysfunction with the release of neuron specific enolase. The significantly higher neuron specific enolase in smokers compared to non-smokers may be due to the harmful constituents of cigarette smoke such as peroxynitrite (ONOO−), which neutralizes NO, resulting in reduced NO bioavailability and generation of more free radicals through (ONOO−) breakdown. Also, UA pro-oxidant activity decreases NO production, leading to vasoconstriction in different tissues, hypoxia and endothelial dysfunction and nerve damage in smokers with the release of neuron specific enolase. This observation is similar to those of Lee et al., (2021) and Janaszak-Jasiecka et al., (2021) who reported an association between endothelial dysfunction driven by hypoxia and the influence of oxygen deficiency on NO bioavailability. The higher serum cotinine, and thiocyanate concentrations in smokers compared to the controls may suggest that both are metabolic products of the constituents of cigarette and may serve as biological markers of exposure to cigarette smoke. Age decreased with increase in smoking pack years, suggesting that the younger experimenting smokers smoke more than the older smokers. There were significant negative correlations between age and cotinine, age and thiocyanate, age and neuron specific enolase, age against smoking pack years, suggesting that the older smokers smoke less compared to the younger ones with decrease in the markers of cigarette smoke exposure and nerve damage in the older smokers cohort. The significant positive correlations between serum thiocyanate and neuron specific enolase, cotinine against smoking pack years, and neuron specific enolase against smoking pack years correspondingly, may suggest a positive association between markers of exposure to cigarette smoke and nerve damage. Limitation of the study: Participants were not screened to rule out other sources of NSE such as small cell lung carcinoma (SCLC) and non-small cell lung cancer (NSCLC). CONCLUSION: This study has shown that smokers have reduced body mass index, uric acid and higher cotinine, thiocyanate and neuron specific enolase levels compared to non-smokers. Both serum thiocyanate and smoking pack years correlated positively with the levels of neuron specific enolase. Neuron specific enolase correlated positively with cotinine levels. Therefore, cigarette smoking may be associated with nerve damage.

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Why is it important?

high levels of cotinine and thiocyanate are associated with increased levels of neuron specific enolase, smoking pack years and decreased uric acid in smokers.