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203
O iginal Resea ch A icle
Monocy e o High Densi y Lipop o ein Choles e ol Ra io in Smoke s
Rode Mam a V.1, Jaiswal Anki a2
1Associa e P o esso , Depa men o Physiology, Go e nmen Medical College, Nagpu , Maha ash a
2Associa e P o esso , Depa men o Physiology, Go e nmen Medical College, Nagpu , Maha ash a
Recei ed: 18-10-2024 / Re ised: 21-11-2024 / Accep ed: 26-12-2024
Co esponding au ho : D . Mam a Rode
Con lic o in e es : Nil
Abs ac :
Backg ound: smoking is a leading cause o mo ali y. Smoking has been linked o low g ade in lamma ion.
Recen ly he monocy e o high densi y lipop o ein choles e ol a io (MHR) eme ged as an indica o o
in lamma ion. So we aimed o in es iga e he ela ionship be ween MHR and ciga e e smoking.
Ma e ial and Me hods: his was Hospi al based c oss sec ional s udy. 25-35 yea s old 200 males we e included
in he s udy & di ided in wo g oups. Smoke g oup comp ising 100 smoke s ha ing du a ion o smoking mo e
han 3 yea s. 100 andomly selec ed non-smoke s we e included in he non-smoke g oup. De ailed his o y,
smoking habi s numbe o ciga e e smoked pe day and pack yea was calcula ed. Comple e blood coun was
done by p ocon PE 600 au oma ed analyze . To al choles e ol, HDL choles e ol, iglyce ide was measu ed on
AU 5800 Backmann coul e ully au oma ed biochemical analyze using enzyma ic colo ime ic assay. S a is ical
analysis was done by unpai ed s uden ' ' es . Co ela ion was de e mined by Pea son co ela ion Coe icien es .
Resul : MHR was signi ican ly highe in smoke s as compa ed o non-smoke s (14.4 + 2.02, 11.1 + 1.98
espec i ely). Pea son's co ela ion analysis e ealed signi ican posi i e co ela ion be ween pack yea s, numbe
o ciga e e smoked daily and MHR in smoke s g oup. Monocy e o high densi y lipop o ein can be used as a
su oga e ma ke o in lamma ion and endo helial dys unc ion.
Keywo ds: smoking, monocy e o high densi y lipop o ein choles e ol a io (MHR) in lamma ion..
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o iginal wo k is p ope ly c edi ed.
In oduc ion
Smoking is he mos impo an public heal h
p oblem acco ding o WHO 2.4 billion people
wo ldwide ha e consumed obacco in he o m o
chewing sni ing o dipping. WHO es ima es
obacco ela ed dea hs o 8.3 million in 2030 and 1
billion dea hs du ing he 21s cen u y [1].
Toxic ing edien s in ciga e e smoke ci cula e
h oughou he body causing damage in se e al
di e en ways. The bu ning obacco and pape
p oduce mo e han 4000 chemical compounds in
o m o gases, apo s pa icula es like ca bon
monoxide hyd ogen cyanide phenols Ammonia
o maldehyde Benzene ni osamines nico ine and a
[2] 194 million man and 45 million women use
obacco in smoke o smokeless o m in India [3].
Smoking has been linked o low g ade sys emic
in lamma ion as e lec ed in ele a ed whi e blood
cell coun a well es ablished p edic o o myoca dial
in a c ion cance and ch onic obs uc i e pulmona y
disease. Ciga e e smoke con ains oxidan ee
adicals ha a e capable o ini ia ing o p omo ing
oxida i e damage leading o degene a i e
pulmona y, ca dio ascula disease and cance [4].
Oxida i e damage o unsa u a ed lipid is a well-
es ablished gene al mechanism o oxidan media ed
cellula inju y [5].
Smoking is associa ed wi h a mo e a he ogenic lipid
p o ile [6] se e al oxins p esen in ciga e e smoke
ha e immunomodula o y e ec s. Ciga e e smoke
cons i uen s induce ch onic in lamma ion a he
mucosal su ace and modi y he hos esponse o
exogenous an igen [7].
The a io o monocy e o high densi y lipop o ein
choles e ol a io was de ined as a ca dio ascula
p ognos ic ma ke indica ing he ex en o
in lamma ion and oxida i e s ess. [7,8,9] So we
planned he s udy o analyze he e ec o ciga e e
smoking and i s in ensi y wi h he lipid p o ile and
MHR a io.
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Mam a V e al. In e na ional Jou nal o Toxicological and Pha macological Resea ch
204
Ma e ial and Me hods
The s udy was app o ed by ins i u ional e hical
commi ee. s udy conduc ed a e ia y Heal h Ca e
Cen e. 200 male pa icipan s aged 25 o 35 yea s
we e included in he s udy. Pa icipan s we e di ided
in wo g oup: 1) smoke g oup comp ised, 100
smoke s ha ing du a ion o smoking mo e han 3
yea s.
2) non-smoke g oup included 100 non-smoke s
selec ed andomly om he gene al popula ion.
Exclusion c i e ia.
Pa ien s wi h p esence o ch onic disease such as
Diabe es melli us, hype ension, co ona y a e y
disease, hea ailu e, ch onic lung disease,
connec i e issue disease, ch onic kidney disease,
me abolic synd ome, leukocy osis, leukopenia o
o he hema ological biochemical o se ological
abno mali ies we e excluded. Subjec s consuming
lipid lowe ing d ugs, s e oids, hema inic we e
excluded.
De ailed da a abou smoking habi s was collec ed
using s uc u al in e iewing ques ionnai es.
Smoking cha ac e is ics such as he numbe o
ciga e es smoked daily, Numbe o Pack yea was
calcula ed. Pack yea ep esen s a combined
measu e o dose and du a ion o smoking. Pack yea
was calcula ed as he numbe o ciga e es smoked
pe day * numbe o yea s smoked / 20.
S anding heigh in cen ime e was measu ed by
asking he pa icipan s o s and ba e ee agains he
wall on which he measu ing scale was insc ibed ( 10
)
Weigh was measu ed in kilog ams wi h KRUPS
weighing machine in ligh weigh ga men s wi hou
oo wea .
Body mass index was calcula ed using Que ele 's
o mula - Body weigh in kilog am / heigh me e
squa ed.
Blood p essu e was measu ed wi h
sphygmomanome e by he s anda d auscul a o y
Ri a Rossi me hod.
Random blood suga was measu ed.
Venus blood sample was collec ed a e 12 hou s o
as ing om he an ecubi al ein wi h all asep ic
p ecau ions. Blood was d awn and ans e ed in o
EDTA and plain bulb equally.
Hema ological pa ame e s we e s udied by P ocan
PE 600 h ee pa di e en ia ed au oma ed
hema ology analyze .
To al choles e ol HDL choles e ol iglyce ide was
measu ed on AU 5800 Backmann coul e ully
au oma ed biochemical analyze .
LDL choles e ol was calcula ed by iedwald
o mula.
S a is ical analysis.
S a is ical analysis was done by so wa e SPSS
e sion 22. Con inuous a iables we e exp essed as
mean and s anda d de ia ion. Analysis was done by
unpai ed ' ' es and co ela ion by Pea son
co ela ion es .
Resul
The mean age, weigh , heigh and body mass index
was ma ched in bo h smoke and non-smoke g oup.
The e was no s a is ical di e ence in age, heigh ,
weigh and body mass index o smoke and
nonsmoke g oup.
The s udy included 200 pa icipan s. I was obse ed
ha monocy e, High densi y lipop o ein Choles e ol
a io alues o he smoke g oup was signi ican ly
highe in smoke s han hose o non-smoke g oup
(Respec i ely14.4+/-2.02 and 11.1+/- 1.98).
T iglyce ide low densi y lipop o ein choles e ol,
o al choles e ol, leukocy e coun monocy e alues
o he smoke g oup we e signi ican ly highe han
hose o he non-smoke g oup.
High densi y lipop o ein choles e ol alue was
signi ican ly less in smoke g oup han non-smoke
g oup.
The e was signi ican posi i e co ela ion be ween
pack yea , numbe o ciga e e smoked daily and
monocy e o high densi y lipop o ein choles e ol
a io.
The e was posi i e co ela ion be ween
T iglyce ide, o al choles e ol, low densi y
lipop o ein choles e ol and pack yea , he numbe o
ciga e e smoked daily in smoke g oup.
The e was nega i e co ela ion be ween high densi y
lipop o ein choles e ol and pack yea s, he numbe
o ciga e e smoked daily in smoke g oup.
Table 1: An h opome ic Cha ac e is ics o Smoke s and non-smoke s
Va iable
Smoke s
Non Smoke s
P alue
Age (yea s)
29.38 + 1.95
28.44 + 1.25
NS
Weigh (kg)
57.68 + 5.07
56.67 + 4.71
NS
Heigh (Cm)
158.58 + 5.03
156.57 + 4.75
NS
BMI kg/m2
23.10 + 1.85
23.28 + 1.54
NS
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Mam a V e al. In e na ional Jou nal o Toxicological and Pha macological Resea ch
205
Table 2: compa ison o Hema ological and lipid p o ile in Smoke s and Non Smoke s
Va iable
Smoke s
Non Smoke s
P alue
WBC X 103/mm3
14.67 + 5.19
8.28 + 3.76
S
Monocy e x 103/mm3
0.75 + 0.53
0.55 + 0.31
S
To al choles e ol mg/dl
194.21 + 12.05
175.38 +11.32
S
T iglyce ide mg/dl
107.12 +25.21
96.12 + 14.25
S
HDL Choles e ol mg/dl
49.01 + 5.47
53.34 + 3.14
S
LDL Choles e ol mg/dl
123.4 + 10.32
106.81 + 8.85
S
Monocy e o HDL Choles e ol
Ra io ( MHR Ra io)
14.4 + 2.02
11.1 + 1.98
S
Table 3: Co ela ion analysis be ween Smoking as pack yea s, MHR & Blood lipid p o ile
Va iable
pack yea s
P Value
MHR
0.254
S
Monocy e x 103/mm3
0.203
S
HDL Choles e ol (mg/dl)
- 0.104
S
T iglyce ide (mg/dl)
0.231
S
To al choles e ol (mg/dl)
0.195
S
Low densi y Lipop o ein choles e ol(mg/dl)
0.198
S
Table 4: Co ela ion analysis be ween he numbe o ciga e es smoked daily MHR and blood lipid le els.
Va iable
The numbe o ciga e es smoked daily
P Value
MHR
0.329
S
Monocy e x 103/mm3
0.295
S
HDL Choles e ol (mg/dl)
-0.279
S
T iglyce ide (mg/dl)
0.293
S
To al choles e ol (mg/dl)
0.105
S
Low densi y Lipop o ein choles e ol
0.132
S
Discussion
In he p esen s udy we ound ha he monocy e o
High densi y lipop o ein a io was signi ican ly
highe in he smoke g oup han non-smoke g oup.
To al choles e ol and T iglyce ides was signi ican ly
highe in he smoke g oup.
Acco ding o se e al ecen s udies exposu e o
ciga e es smoke impai s unc ional s uc u e o
endo helial cells. Nico ine and inc ease oxida i e
s ess gene a ed om smoking induce ascula
endo helial dys unc ion ia he inhibi ion o
endo helial ni ic oxide syn hase and dec easing
gene a ion o ni ic oxide [10,11].
Nico ine inc eases he exp ession o adhesion
molecules in endo helial cells such as E selec and
in acellula adhesion molecule because o enhanced
a achmen and ansmig a ion o monocy es in he
essel wall. [12].
I is e iden ha hese esul s sugges ha smoking
is an es ablished isk ac o o a he oscle osis
h ough se e al unde lying pa hways. Monocy es
a e a dis inc ype o leukocy es which ha e a key
ole in in lamma ion and a he oscle osis p ocess
[13].
Ac i a ed monocy es in e ac wi h damaged o
ac i a ed endo helium which esul in o e
exp ession o p o in lamma o y cy okines / adhesion
molecules and in acellula adhesion molecule.
The e a e monocy es di e en ia e in o he
mac ophages ha inges oxidized LDL-C and o m
dange ous oamy cells[14].
In ano he s udy The Coun o ci cula ing monocy es
was ound o be a p edic o o new plaque
de elopmen as well. [15] howe e HDL-C ea u es
an i-in lamma o y an ioxidan s and an i h ombo ic
e ec . [14.16.17] HDL- C can p e en in lamma o y
esponse by ac ing di ec ly on monocy es. Recen
s udies indica e he ole o HDL -C in modula ing
monocy e ac i a ion adhesion and in con olling he
p oli e a ion o p ogeni o cells ha di e en ia e o
monocy e. HDL-C also p ohibi s oxida ion o LDL-
C IN addi ion o inhibi ion o mac ophages
mig a ion. I also emo ed oxidized LDL-C om
oamy cells. [16,17,18,19,20].
The e o e monocy es show a p o in lamma o y
e ec bu HDL-C unc ions as e e sal ac o du ing
he p ocess. I has been sugges ed ha MHR has a
ela ionship wi h sys emic in lamma ion and
endo helial dys unc ion and i is accep ed as newly
ecognized in lamma ion based diagnos ic and
p ognos ic ma ke in ca dio ascula disease
[21,22,23,24]. Recen ly Acikgoz e all assessed
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Mam a V e al. In e na ional Jou nal o Toxicological and Pha macological Resea ch
206
endo helial unc ions using low and ni oglyce ine
media ed dila ion echnique and calcula ion o
MHR. The s udy epo ed he e was a s ong in e se
co ela ion be ween MHR and low
media ed dila a ion. The e o e ele a ed MHR may
be a use ul ma ke e lec ing impai ed endo helial
unc ion and sys emic in lamma ion[25].
The ela ionship be ween smoking
sys emic in lamma o y esponse, ascula
endo helial inju y and a he oscle osis has been well
de ined
MHR can be used as a su oga e ma ke o
in lamma ion and endo helial dys unc ion.
Conclusion
MHR is a simple easy cos -e ec i e ool ha should
be used o p edic ing he sys emic in lamma o y
esponse and possible endo helial dys unc ion in
smoke s. Cases wi h high MHR can easily be
iden i ied du ing ou ine comple e blood analysis
and could possibly bene i om p e en i e
ea men . The e o e mo e a en ion should be gi en
o hese indices in he examina ion o smoke s.
Decla a ion by Au ho s
E hical App o al : App o ed
Acknowledgemen : None
Sou ce o unding : None
Con lic o In e es : The au ho s decla e no con lic
o in e es
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