Abstract

Smoking of cigarettes worsens morbidity and mortality rates by prompting cancer, pulmonary, cardiovascular, and oral diseases. Despite having all these severe risks of smoking, the habit is unacceptably widespread, particularly among teenagers in many countries, including Bangladesh. In this investigation, the acute effect of cigarette smoking on oxidative stress and inflammation (Tumor Necrosis Factor- α (TNF-α)) has been analyzed in the cigarette smoke (CS)-exposed rats. Exposure of smoke in vivo significantly increased the levels of Lipid Peroxide (LPO) and TNFα in the experimental rats, when compared to those of the control rats. Furthermore, washed erythrocytes isolated from control rats were exposed directly to CS in vitro. The time-dependent exposure of smoke to erythrocytes increased the oxidative stress in the erythrocytes, as indicated by increased levels of LPO in the erythrocytes. The toxic effect of acute cigarette smoke was also visible in the morphological studies of erythrocytes. Cigarette smoke-exposed erythrocytes revealed numerous leakage, breaks and membrane blobs in the plasma membrane of erythrocytes. Our results thus suggest that cigarette smoke not only affects the lung tissues but may also deteriorate the morphology of erythrocytes by instigating the oxidative stress in the erythrocytes.

Highlights

  • Chronic cigarette smoke exposure is well-known for its detrimental effects on lung and erythrocyte

  • In vitro exposure of erythrocytes to smoke increases the level of hemolysis and time-dependent oxidative stress as indicated by the increased extent of Lipid Peroxides (LPO) in the erythrocytes than those in the un-exposed erythrocytes under experimentation (Figures 2A and 2B)

  • In case of in vivo exposure to smoke there is no significant induction on the level of erythrocytes hemolysis between the smoke exposed and the control rat group

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Summary

Introduction

Chronic cigarette smoke exposure is well-known for its detrimental effects on lung and erythrocyte. An acute smoking model is a reasonably easier and more sensitive method of scrutinizing the specific effects of cigarette smoke on oxidative stress and inflammatory response. Cigarette smoke is a source of Reactive Oxygen Species (ROS) such as superoxide anions, hydroxyl radicals, hydrogen peroxide, metallic ions and quinones. These oxidizing agents can upsurge the levels of oxidative stress in the smokers (Pryor and Stone, 1993; and Marnett et al, 2003) with increased Lipid Peroxides (LPO) contents and degradation products of extracellular matrix proteins (Van der Vaar et al, 2004). ROS present in cigarette smoke are responsible for cellular injury and inflammation (Khan et al, 2014)

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