The Expression Of PCNA and Apoptosis On Liver Cell Damage Due To Oxidative Process Of Aflatoxin B1 Biotrans Formation.
Process
on Liver Cell Damage due to Oxidative
Apoptosis
ancl
PCNA
of
The Expression
of nflatoxin Br Biotrans Formation
YANWIRASTI
Facultl'Andalas []niversit]" Padang-lrrdonesia
Department of Anatom,v. Medical
ABSTRACT
cell Nuclear
disclose the expression of: Proliferative
The objective of this study was to
produced by
process
*ttit. *t;'liver cells due to oxidati'e
Antigen (PCNA)
factorial desig.
9n
"";;;;o.ri,
orRnuto*in Br biotransrormation. Using
times
exposnre
and
dosages
different
used' J'hc
times and four dosages o1'AIrB1 wele
in this experimental study three exposure
of 24
groups
four
healthy t"Iit: rats were dlvided into
Aduit
rats.
;ffi
96
used
experiment
further into three sub
of ar.n. given. Each.groups was divided
rats each. based on the dosages
leghth olt*po'u" time to AFBr'
rur,
"titr'e
orally every day into ditferent groups'
-o.z
Four dosages of AFBr. *.r. int',oauced
nrl propyiene glicor. Three subgroup received
dissorv.a'i"
20.
i!
lo.
0.
of
consisted
""al6 weeks una zo weeks. At the er-rd of the experiment. the rats were
the dosage for l2;;.
pCNA *ere rcruti'ized using immunohistochemicar method. 'sing
with
ceils
Liver
sacrificed.
d-ete''i'ed by using apoprag merhod
ovidin biotin rnethod (DAKO) *d "p;;;;;is .*.r.
histological
*'n;te liver cell damage were examined using
(peroxidase i'situ io..,ion tii).
,ii.., ,tuin.d by haematoxillin eosin'
of PcNA rvere signihcant dift-erenccs between
our data conflrmed that : 1) Ilxpression
started)'
oni tS pg AFBl exposure 1a time that dysplacia
2)
no exposure AFBr with 16 weeks
o1'AFBr'
inc"reasing dosages and-time.exposure
(a
time
The expression become increase. uy itr.
exposLlre
in.r.ur.a until ldweeks-and l5 pg AFBr
Expression of apoptosis become
dosage a.d
increasing
by the
that therc is no increase anymore
that dysplaciu ,turt.a-i^[u, un.,
time exposu'l,.ffi""clude
u.til a timc
that the exprcssion..olil?lt:ti'
pc:NA bsconre increase aticr a rime r'r'hcre
ir.,ui. whire
ori.r
J.crease
*iir
srarred.
dyspracia
^J
dysplacis started.
;;;;;i;ign,
i*tJ
!:::.ll:^:::':"t'
Aflatoxin Br
Key words : PCNA' apoptosis'
on Liver Cell Damage due to Oxidative
Apoptosis
ancl
PCNA
of
The Expression
of nflatoxin Br Biotrans Formation
YANWIRASTI
Facultl'Andalas []niversit]" Padang-lrrdonesia
Department of Anatom,v. Medical
ABSTRACT
cell Nuclear
disclose the expression of: Proliferative
The objective of this study was to
produced by
process
*ttit. *t;'liver cells due to oxidati'e
Antigen (PCNA)
factorial desig.
9n
"";;;;o.ri,
orRnuto*in Br biotransrormation. Using
times
exposnre
and
dosages
different
used' J'hc
times and four dosages o1'AIrB1 wele
in this experimental study three exposure
of 24
groups
four
healthy t"Iit: rats were dlvided into
Aduit
rats.
;ffi
96
used
experiment
further into three sub
of ar.n. given. Each.groups was divided
rats each. based on the dosages
leghth olt*po'u" time to AFBr'
rur,
"titr'e
orally every day into ditferent groups'
-o.z
Four dosages of AFBr. *.r. int',oauced
nrl propyiene glicor. Three subgroup received
dissorv.a'i"
20.
i!
lo.
0.
of
consisted
""al6 weeks una zo weeks. At the er-rd of the experiment. the rats were
the dosage for l2;;.
pCNA *ere rcruti'ized using immunohistochemicar method. 'sing
with
ceils
Liver
sacrificed.
d-ete''i'ed by using apoprag merhod
ovidin biotin rnethod (DAKO) *d "p;;;;;is .*.r.
histological
*'n;te liver cell damage were examined using
(peroxidase i'situ io..,ion tii).
,ii.., ,tuin.d by haematoxillin eosin'
of PcNA rvere signihcant dift-erenccs between
our data conflrmed that : 1) Ilxpression
started)'
oni tS pg AFBl exposure 1a time that dysplacia
2)
no exposure AFBr with 16 weeks
o1'AFBr'
inc"reasing dosages and-time.exposure
(a
time
The expression become increase. uy itr.
exposLlre
in.r.ur.a until ldweeks-and l5 pg AFBr
Expression of apoptosis become
dosage a.d
increasing
by the
that therc is no increase anymore
that dysplaciu ,turt.a-i^[u, un.,
time exposu'l,.ffi""clude
u.til a timc
that the exprcssion..olil?lt:ti'
pc:NA bsconre increase aticr a rime r'r'hcre
ir.,ui. whire
ori.r
J.crease
*iir
srarred.
dyspracia
^J
dysplacis started.
;;;;;i;ign,
i*tJ
!:::.ll:^:::':"t'
Aflatoxin Br
Key words : PCNA' apoptosis'