Chronic cigarette smoking alters erythrocyte membrane lipid composition and properties in male human volunteers

Cigarette smoking impairs Na+-K+-ATPase activity in the human coronary microcirculation

“…Recent studies (14,47) have proposed in VSMCs that the phosphotidyl inositol 3-kinase (PI3K)/Akt pathway is associated with the increase in the transcript and with protein translocation to the cell membrane. Importantly, chronic smoking causes impairment of Na ϩ -K ϩ -ATPase activity in human erythrocytes and platelets, coinciding with altered membrane properties such as membrane lipid peroxidation, an increase in the ratio of cholesterol and phospholipid, and an decrease in membrane fluidity (35,36). An in vivo study (44) of canines subjected to chronic cigarette smoking also showed impaired Na ϩ -K ϩ -ATPase activity with similar alterations in the microenvironment of the VSMC membrane.…”

Cigarette smokers develop structurally modified hemoglobin: a possible way of increasing oxidative stress

“…Previous studies indicate that smokers in comparison with non-smokers show increase in hematocrit value, red cell count, mean corpuscular volume, white cell (total and differential) counts (Kim et al, 2007;Kurata, 2006;Tollerud et al, 1989) along with increased hemoglobin concentration (Bain et al, 1992;Norton & Rand, 1981;Suwazono et al, 2010). It has also been reported that the smoking-induced generation of reactive species may alter fatty acid composition and physical property of erythrocyte membrane (Padmavathi et al, 2010;Pretorius et al, 2013). Recently, Pretorius et al (2013), in an investigation using high-resolution scanning electron and atomic force microscopy reveals that there is significant change in red cell morphology among cigarette smokers.…”

“…(Ambrose & Barua, 2004), which are capable of causing an increase in generation of various reactive species, specially reactive oxygen species (ROS). Therefore, by each puff one smoker is exposed to a free radical load by such oxidizing agents (Padmavathi et al, 2010) with an estimation of 10 15 free radicals per puff (Church & Pryor, 1985). Due to extreme reactivity, the ROS may react with many compounds in the neighborhood.…”

Secondhand Smoke Is an Important Modifiable Risk Factor in Sickle Cell Disease: A Review of the Current Literature and Areas for Future Research

“…For example, TSE, including secondhand smoke, is known to increase pro-inflammatory mediators, up-regulate cellular adhesion factors, damage platelets and endothelium [59,60,61,62], and increase hemolysis of red blood cells [62,63,64,65], all of which contribute to SCD vaso-occlusion and end-organ complications [66]. Hemolysis and free hemoglobin released from lysed red blood cells have also been associated with SCD morbidity and end-organ complications, such as pulmonary hypertension [67].…”

“…Hemolysis and free hemoglobin released from lysed red blood cells have also been associated with SCD morbidity and end-organ complications, such as pulmonary hypertension [67]. There are some data to suggest that cigarette smoke introduces oxidative stress and induces alterations of the erythrocyte membrane lipid composition and leads to increased erythrocyte fragility and hemolysis in smoking adults without SCD, [62,63,65] though this has not been studied in people with SCD. A similar effect has been seen in rabbit erythrocytes (i.e., tobacco smoke induced hemolysis) [64].…”