ON TESTIS AND EPlDlDYMlS OF RATS - Pondicherry University ...

Fin. L Corrclatwn bclwfcn "perm counts and DNA cootent$ or
Fil. 7. Urea of TCDD on lied mlidrtion in the s~ididvrnal nl cpididymli rprm. A paaltivc corrclaten (r-0.9% n-24) war
Grin or la.. 7hc m m adktyu in m~rdm.i"
found between rprm wunl and DNA contcnl
pr
mtnulc and rnillignnn or mein Ot millisnm 01 DNA. n o data
urn n W M munlSD Iw ax uprimcnUl and am control
mum. PcO.05 lm~erldx) il lo indiate a rienificant activity (Kono and Fridovich 1982). Cataiasc or
glutathione peroxidae rails to eliminate HZ02 from the
cell, and the accumulated H202 has been shown to cause
inactivation of superoxidc dismutase (Sine1 and Garber
1981). Griveau and Lannou (1997) reported lhal ROS
dovl of TCDD (0.15 ndkg per day on 5 days/week for
13 weeks) wuld induce oxidative stmu in liver, spleen,
lung and kidncy following rubchronic exposure in mice
(Skwk ct ill. WOO). In tho orrscat rtudv administration
of TCDD cuuml II ducll& In the sperin wunts, which
1s wnrrclcnl wtth esrlter reporu (Fwt el al 1991. Gra)
cl uI 1997) S~nce a wry ugn~hcrat wrnlauon (r- 0 95.
18-24) was ohncrvfd bitwan cprm counb and DNA
conlcnb in cpididyntnl,sperm. DNA wnlcnt wus routinely
ucsd M an indicator of sprm wunt (Mukherja
cl ul. 19921. Adminiatnlion of TCDD decreased the
hydrogen peroxide and lipid peroddauon roo in the
enididvmal soerm of mla in tams of boLb ~mlcin and
~ N *LI~~I; A doso-response wsr not obscr;od wtl! re.
galrd lo .any ofllr hit)~.hw~luI ptmmctcn In our rlvdx\.
which is auito similar to (he mulb obrwed in studies of
the ctTcct.of TCDD on the hepatic and braln tluues of
nu ( Hmun el d. 2001). M~tochondnPl mplntlon tr
the main biolo+icnl mum of tuamxidc anion radials
in physiolopi&l conditions. 7% antioxidant snrymc
superoxide dimuusc lsaknla the diimuulion of Ihc
runeroxidc anion into hvdroncn mxidc. Cnlal;~se ilc-
such as HIOl appear to be key agents in the cytoloxic
elTects in spennalozoa, and in addition lo their direct
erect on the cellular wnstimcnt, to produce oxida~ve
stress by darcasing the enzymatic defenses. Thc rise in
the kvels of hydrogen peroxide generation by 160-170%
reflccls the induction bv TCDD of the oroduction of
mctlve oxygen rpcctcs~lhat arc no1 e.ttn'~nated b\ lhr
ant~oxtdanc enzyme, rush as catalase and g.u~ath~one
reductase/proxidase systems, and this can induce lipid
oeroxidation. The wssibilitv of eflects other than the
uppnrcnt darease In unt!oa~d.lnt actl\lltcs tn caus ng 1hc
tncw m peroude product.on also cdnnol bs r~lcd
our. Cytoplasm of the spermatozoa is extremely limited
in volume and localization. so that the ~olvunsaturated
fatty aads lhsl nhound In Ihe eprm plkm'a mcmnrd.w
urc vcry suscept~blc to ROS ultdck (Al.kcn et ul tYSJ,
When ROS &nczntrationr are high, predamaged spcrmatozoa
are exposed to lipid peroxidation by polyunsatunlcd
fatty acids (Ichikawa el al. 1999). The sperm
membranes have been teported to undergo permeabilily
chanua followinn enhanced linid mroxidation and
glut~htone deplc