Asian Pacific Journal of Tropical Disease (2011)289-291

289

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Asian Pacific Journal of Tropical Disease

journal homepage:www.elsevier.com/locate/apjtd

Document heading

Evaluation of effect of smoking and hypertension on serum lipid profile

and oxidative stress
Jeeyar1, Hemalatha2, Wilma Delphine Silvia CR3*
Department of Biochemistry, KMCT Medical College, Calicut-673602
Department of Biochemistry, Dr.BR. Ambedkar Medical College, Bangalore-560045
3
Department of Biochemistry, Sapthagiri Institute of Medical Sciences & Research Center, Bangalore-560090, India
1
2

ARTICLE INFO

ABSTRACT

Article history:
Received 18 August 2011
Received in revised form 27 September
Accepted 20 October 2011
Available online 28 December 2011

Objective: To determine the effect of smoking, hypertension individually on lipid profile and
lipid peroxidation and the cumulative influence of smoking and hypertension on oxidative stress
and lipid profile. Methods: Serum total cholesterol, high density lipoprotein (HDL), low density
lipoprotein (LDL), very low density lipoprotein (VLDL), triglycerides and malondialdehyde (MDA)
were estimated in sixty cases including twenty smokers, twenty hypertensives, and twenty
smokers with hypertension and compared with those in twenty age and sex matched healthy
controls. Results: Statistically significant increase in MDA, total cholesterol, LDL, VLDL and
triglycerides and decrease in HDL in cases were observed in smokers, hypertensives and smokers
with hypertension when compared to healthy controls. Smokers had significantly elevated levels
of lipid profile and MDA except for HDL when compared to hypertensive group. Statistically
significant increase in the levels of study parameters of smoking and hypertensive group was
noticed when compared to group with hypertensives (P<0.05) and there was a statistically
significant decrease in HDL levels in smoking and hypertensive group when compared to healthy
controls. All the biochemical study parameters had larger effects (0.80<d<1.20) for the smoking
and hypertensive group in comparison with control group. Conclusions: Cigarette smoking,
together with hypertension, has larger effect on lipid profile than in patients with cigarette
smoking or hypertension alone and induces alteration in serum lipid levels and oxidative stress
in the direction of increased risk for coronary artery disease.

Keywords:
Smoking
Hypertension
Lipid profile
Malondialdehyde
Oxidative stress
Lipid peroxidation
Total cholesterol
HDL
LDL
Triglycerides
VLDL

2011

1. Introduction
Cigarette smoking is acknowledged as one of the leading
causes of preventable morbidity and mortality, and is
one of the largest preventable causes of ill health in the
world. Cigarette smoking is said to be responsible for
17%-30% of all deaths from cardiovascular illness. The
effects of cigarette smoking are dose-related and life style
modification measures involving quitting smoking are
probably the single most important steps to decrease the
chance of coronary artery disease and a heart attack[1].
D yslipidemia, a strong predictor of cardiovascular
disease, which causes endothelial damage and the loss
of physiological vasomotor activity that results from
endothelial damage may become manifested as blood
*Corresponding author: Dr. Wilma Delphine Silvia CR, MBBS., MD., DNB., Professor
and Head, Department of Biochemistry, Sapthagiri Institute of Medical Sciences and
R esearch C enter, # 15 , C hikkasandra, H esaraghatta M ain R oad B angalore 560090 ,
Karnataka, India.
Tel: 09448169967
E-mail: widel2008@gmail.com, widel@rediffmail.com

pressure increases. Therefore, factors like dyslipidemia that

cause endothelial dysfunction may lead to hypertension[2].
P lasma lipoprotein abnormalities are said to be the
underlying major risk factors and may even be essential
for the common occurrence of atherosclerotic vascular
diseases[3]. Free radical mediated lipid peroxidation has
been associated with the pathogenesis of many diseases and
clinical conditions. Oxidative pathway appears to be one
important mechanism for modifying low density lipoprotein
(LDL), because a wide variety of structurally unrelated
antioxidants inhibit atherosclerosis. Lipid peroxidation is
one of the pathological processes impairing the function of
arterial endothelial cells. Oxidative damage to unsaturated
lipids is a well established, general mechanism for oxidant
mediated cellular injury. Oxidative stress appears to be
a probable clinically relevant factor in cigarette smokerelated atherogenesis and increased lipid peroxidation is
also a risk factor for myocardial infarction[4].
H ypertension is a risk factor for the development
of atherosclerosis. T here is increasing evidence that
atherosclerosis should be viewed fundamentally as
an inflammatory disease. Atherogenic stimuli such as

290

Jeeyar et al./Asian Paicfic Journal of Tropical Disease (2011)289-291

hyperlipidemia appear to activate the inflammatory response

by causing expression of mononuclear leukocyte recruiting
mechanisms. Hypertension not only is a well-established
cardiovascular risk factor but also increases the risk of
atherosclerosis. Both of hypertension and dyslipidemia
are independent risk factors for the development of
atherosclerosis[5]. Though individually these two factors
are known to have adverse effects on lipid profile and lipid
peroxidation, there are limited studies to substantiate their
cumulative influence on oxidative stress and lipid profile.
Hence, the present study was aimed to find the collective
effects of cigarette smoking and hypertension on lipid profile
and lipid peroxidation.
2. Materials and methods
Eighty subjects were included in this study, out of which
twenty healthy subjects were considered as group I who
were nonsmokers and nonhypertensives, aged between
35 to 55 years as controls and whereas cases were age and
sex matched sixty subjects who were enrolled from the
Outpatient Department of Medicine. These sixty subjects
were divided into 3 groups. The criteria for chronic smokers
were taken as those who smoked more than 10 cigarettes
per day for more than 10 years (10 pack years)[6]. The criteria
for hypertension were taken as those who were having
average blood pressure of 140/90 for a period of more than
10 years[6]. Twenty chronic smokers were included in group
II. Hypertensives were included in group III but are not
smokers. Twenty chronic smokers with high blood pressure
were included in group IV. Patients with renal disorders,
diabetes mellitus, liver disorders and other chronic
infections and those who were on antioxidants or vasoactive
medications were excluded from the study. Informed consent
was taken from each patient and the study was approved by
Institutional Ethical Committee.
A volume of 5 mL of fasting venous blood sample was

collected with aseptic precautions. Blood samples were

allowed for clotting. Serum was then separated and analyzed
for lipid profile and malondialdehyde (MDA) levels. Serum
total cholesterol (TC) was estimated by the method of Zak.
high density lipoprotein cholesterol (HDL-C) was estimated
by the precipitation method. Serum triglyceride (TG) was
estimated colorimetrically using the Hantzsch reaction[7].
Very low density lipoprotein cholesterol (VLDL-C) was
calculated by using the formula of Rifai and Warnick[8].
Measurement of by-product of lipid peroxidation, MDA was
done by thiobarbituric acid method[9].
The statistical software SPSS 11.0 was used for the analysis
of the data and Microsoft Word and Excel have been used
to generate tables. The analysis of variance (ANOVA) has
been used to find the significance of mean of lipid profile
and MDA between group I, group II, group III and group IV.
P<0.05 was considered as statistically significant.
3. Results
Statistically significant increase was found in serum TC,
TG, VLDL and LDL-C of sixty cases together and each

group of cases and serum parameters were compared with

those in control group (P<0.001 and P<0.05) except for MDA
levels between group III and group I. Statistically significant
decrease in HDL in each group of cases was observed when
compared to controls. When the levels of all the parameters
in this study were compared between smokers ( group
II) and hypertensives (group III), statistically significant
higher elevated levels of lipid profile were found in chronic
smokers than hypertensive individuals (P<0.05) except for
HDL. Statistically significant greater increase in the levels
of study parameters of group IV subjects with risk factors of
smoking and hypertension was noticed when compared to
group III with hypertensives (P<0.05) excepte for HDL (Table
1). All the lipid parameters and MDA had larger effects
(0.80<d<1.20) for group IV in comparison with control group.

Table 1
Mean pattern and comparison of lipid profile and MDA in cases and controls (meanSD).
Parameters
TC
TG
HDL
LDL
VLDL
MDA

Group I

Group II

167.0512.43

225.2018.11

45.853.86

34.951.39

123.3516.48
24.173.20

Group III

215.508.87

a***

218.0015.42

203.008.64

147.3517.50

125.407.14

a***

a***

100.3517.20
2.370.03

a***

42.902.49
2.460.06

a***

a***

a***

ab***

37.001.52

ab***

ab***

40.601.73
2.380.03

ab***

b***

Group IV

244.5019.59

abc***

221.5014.24
35.002.29

ac***

ac***

142.4011.65
44.302.85

ac***

ac***

2.490.03

ac***

F value
91.910

216.007
87.907
44.530

253.215
49.749

: P<0.05 as compared with group I; : P<0.05 as compared with group II; : P<0.05 as compared with group III; ***: P<0.001 as compared with group I.

4. Discussion
Atherosclerosis is the underlying process involved in
coronary artery disease, peripheral vascular disease and
stroke[10]. Smoking causes a huge and increasing number of
untimely deaths in India[11]. There are currently 240 million
tobacco users aged 15 years and above (195 million male
users and 45 million female users) in India. The prevalence
of tobacco use is higher in rural population than that in
urban areas[12].

T he biological mechanisms linking smoking and

atherogenesis are complex and not fully understood. In
addition to inflammation, potential mechanisms by which
smoking increases the risk of cardiovascular diseases
include systemic haemostatic and coagulatory disturbances,
lipid abnormalities, increase in oxidative stress, and
vascular endothelial dysfunction[13]. Cigarette smoking
leads to increase in the concentration of serum TC, LDL-C,
TG, VLDL-C, and fall in the levels of anti-atherogenic
HDL - C [14] . I t is presumed that nicotine stimulates
sympathetic adrenal system leading to increased secretion
of catecholamines resulting in increased lipolysis and

Jeeyar et al./Asian Paicfic Journal of Tropical Disease (2011)289-291

increased concentration of plasma free fattyacids, which

further results in increased synthesis of hepatic TG, along
with VLDL-C in the blood stream[15]. Cigarette smoking is
associated with higher androstenedione levels, a higher total
androgen to total estrogen ratio, and lower progesterone
levels[16].
High levels of LDL-C, VLDL-C, and TG are strongly
associated with the development of coronary artery
disease, while a low level of HDL-C remains a significant
independent predictor of coronary artery disease[17].
Hypertension is one of the major risk factors for coronary
artery disease and stroke. Hypertension is an independent
risk factor for atherosclerosis. I t is well known that
hypertension is associated with abnormal changes in lipid
profile (dyslipidemia) which is a cause for atherosclerosis[18].
Cigarette smoking and hypertension individually potentiates
lipid abnormalities but the combined effect has to be
studied.
Tobacco smoke contains large numbers of free radicals
that are capable of initiating or promoting oxidative injury.
Cigarette smokers have higher lipid peroxidation products
in their blood when compared to nonsmokers and smoking
increases the concentration of serum MDA levels[14]. It is
suggested that oxidative injury may play a major role in
mediating the health risks associated with cigarette smoking.
Oxidation of LDL might be an important mechanism whereby
cigarette smoking can accelerate atherogenesis. LDL from
smokers was more susceptible to peroxidative modification
when compared to that from non-smokers[14]. There is
evidence to suggest that oxidatively modified LDL may
contribute to the pathogenesis of atherosclerosis[19].
Both cigarette smoking and hypertension are proven
independent risk factors for atherosclerosis; both are
associated with abnormalities in lipid profile and also show
high values of serum MDA indicating increased rate of
lipid peroxidation which suggests involvement of high rate
of oxidative stress. Though theoretically we can assume
that there is a cumulative effect of both cigarette smoking
and hypertension on these cardiovascular risk factors.
From this study, it is well established that in both cigarette
smoking and hypertension there is dyslipidemia and
increased oxidative stress. The constellation of these altered
lipoproteins along with lipid peroxides suggests that smokers
with hypertension are at a high risk for the development of
coronary heart disease.
There is a cumulative effect of cigarette smoking and
hypertension on lipid profile and lipid peroxidation,
indicated by increased levels of serum MDA and
dyslipidemia indicated by higher values of TC, TG, LDL,
VLDL , and lower levels of cardio protective HDL . T his
observation suggests that there is a more risk of progression
of atherosclerosis in individuals who have both the risk
factors i.e. smoking and hypertension. F urther large
population studies are required to substantiate our findings.
Conflict of interest statement
We declare that we have no conflict of interest.

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