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

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apidly proliferating cells of testis reflects the initial phase ol' sper~iiiltoycncsis including spermatogonial proliferation by mitosis and the onset of meiotic prophase in prc-leptotcne primary spermatocylcs (Monesi, 1965). ItNA synthesis is highost during the mid pachytene phase and the end of the meiotic prophase and mRNA specific for structural protein increases during prophase of meiosis (Slaughter el 01.. 1989). The rate of protein synthesis has been reported to be higher in type A spermatogonia than in type B (Monesi, 1965). Toxicants that would alter mitosis or differentiation of spermatogonia would be expected to have a major influence on the efficiency and total productivity of spermatogenesis. 1.1.1.2 Hormonal control of spermatogenesis There is general agreement that for quantitatively normal spermatogenesis to occur, testis requires stimulation by pituitary gonadotrophins such as follicle stimulating hormone (FSH) and luteinizing hormone (LH). The progressive rise of FSH and LH during sexual maturation has been reported in humans and in other animals (for review, see de Kretser et ul., 1998). FSH and LH have been shown to stimulate seminiferous tubules and reinstate spermatogenesis in hypophysectomized rats (Greep and Fevold, 1937). Synergistic action of FSH and testosterone for the maintenance of spermatogenesis has also been reported (Steinberger. 1971). In the prepubertal rat, FSH alone is required to maintain testicular growth (Courot el al., 1970) and synthetic activity of Senoli cells (Means et al., 1976). High intratesticular concentrations of testosterone are required for normal spermatogenesis. Testosterone has been shown to act by stimulating Senoli cells and receptors for FSH are located on the Senoli cells and spermatogonia. FSH has been shown to exert its action via CAMP. Injection of FSH is associated with a stimulation of protein kinase activity and protein synthesis. FSH has been shown to play a role in stimulating mitotic and meiotic DNA synthesis in type B spermatogonia and pre-ieptotene spermatocytes as well as in preventing apoptosis of pachytene spermatocytes and round spermatids (Henricksen el ul.. 1996: Shetty el ul.. 1996). Mc lachlnn el ol. (1995) detnonstrntod that FSH alone could partially restore spermatogenesis in GnRH-immunized rats.
lmn~unization of monkeys against FSH either actively or passively has been shown to be associated with disruption of fertility and a decline in sperm concentrations. It has been reported that the specific spermatogonial subtypes are affected by withdrawal of FSH alone (Moudgal et al., 1997). FSH has been shown to promote spermatogenesis and fertility in primates (Moudgal and Sairam, 1998). Administration of highly purified FSH to GnRH antagonist treated monkeys has been shown to niaintnin spermatogonial numbers (Weinbauer el a/., 1991). Actions of FSI-I on Sertoli cells from prepubertal animals have been reported biochemically by increased estradiol production (Fritz et al., 1976). It has been reported that FSH P-subunit gene knocked out mice. rendering them FSH deficient showed that spermatogenesis could proceed to completion albeit in the presence of smaller testes (Kumar et al., 1997). The binding of LH to Leydig cells in the interstitial compartment of testis has been reported to stimulate testosterone synthesis. Initiation of spermatogenesis by testosterone and dehydrotestosterone has been reported in mouse (Singh el al.. 1995). Testosterone alone has been shown to maintain spermatogenesis qualitatively in a dose-dependent fashion in monkeys (Weinhnuer el (11.. 1988). A high concentration of tcstosteronc within thc seminiferous tubules LH has been shown to play a role in the initiation and maintenance of sperm production in mouse (di Zerega and Sherins, 1980; Matsumota and Bremmer. 1987). In rodents and primates, by virtue of its local production. intratesticular testosterone levels have been shown to be elevated approximately 100 fold above those in serum (Huhtaniemi er al., 1987). A role for estrogens in normal spermatogenesis has also been reported (Hess ef ul.. 1997) and at least two major steps have been shown to be influenced by estrogens in the seminiferous tubules, stem cell number and spermatid maturation (Hess cr ul., 1997). It has been shown that in virro multiplicntion of rat gonocytes is controlled by growth factors and estradiol, which corresponds well with the presence of ERP in these cells (Hess et a!., 2000). In estrogen receptor a knockout (ERKOa) mouse estrogens are necessary for the achievement of fertility (Hess et al.. 2000).
Page 1 and 2: FUNCTIONAL STUDIES ON THE EFFECTS O
Page 3 and 4: ACKNOWLEDGEMENTS I wish to express
Page 5 and 6: TABLE OF CONTENTS Page No ACKNOWLED
Page 7 and 8: TABLE OF CONTENTS (Continued) Deter
Page 9 and 10: TABLE OF CONTENTS (Continued) Effec
Page 11 and 12: TAULIC OF CON'I'ISN'I'S (C'untinued
Page 13 and 14: xi LIST OF TABLES (Continued) I'agc
Page 15 and 16: Table 24a Table 24b Table 24c Table
Page 17 and 18: Fig. 1 Fig. 2 Effect of TCDD on the
Page 19 and 20: Fig. 12c Fig. 12d Fig. 13 Fig. 14a
Page 21 and 22: LIST OF FIGURES (Continued) Fig. 23
Page 23 and 24: LH M PL mg mRNA N AD NADH NADP NADP
Page 25 and 26: layers, an outer layer of visceral
Page 27: tubular epithelium and continually
Page 31 and 32: and this reaction is catalyzed by t
Page 33 and 34: extratubular environment or synthes
Page 35 and 36: the most active in protein secretio
Page 37 and 38: 1958). A rapid fall in serum testos
Page 39 and 40: have also been reported in the rats
Page 41 and 42: Effect of TCDD on heart muscle has
Page 43 and 44: 1.4 Effect of oxidative stress on m
Page 45 and 46: 2 SCOPE OF THE PRESENT STUDY There
Page 47 and 48: 3 MATERIALS AND METHODS 3.1 Animals
Page 49 and 50: Subgroup III: Administration of TCD
Page 51 and 52: choppcd with the help of sharp razo
Page 53 and 54: anti-FSH antibody. After incubation
Page 55 and 56: lust sped (500 to 700 rpm) on an or
Page 57 and 58: 3.13.4 Quantitative determinntiun u
Page 59 and 60: The plates were dried by inverting
Page 61 and 62: centrifuged at 3,500 g for I5 min o
Page 63 and 64: 3.17 Preparation of tiasue humogena
Page 65 and 66: supcrnutant was taken. Hlunk was pr
Page 67 and 68: 3.21.4 Assay of glutathione peroxid
Page 69: 4 RESULTS 4.1 Administration of TCD
Page 72 and 73: seminiferous tubules was found to b
Page 74 and 75: fractions of rat testis as compared
Page 76 and 77: 4.1.11.1 Effect of TCDD on the prod
Page 78 and 79:
4.2 Co-administration of TCDD and v
Page 80 and 81:
4.2.8 Effect of co-administration o
Page 82 and 83:
4.2.11.5 Effect of co-administratio
Page 84 and 85:
Table I b. Effect of TCDD on the we
Page 86 and 87:
Table 4. Effect of TCDD on the seru
Page 88 and 89:
Table 7b. Effect of TCDD on the pro
Page 90 and 91:
Table 8c. Effect of TCDD on the lev
Page 92 and 93:
Table 9d. Effect of TCDD on the act
Page 94 and 95:
Table 13. Effect of TCDD on the ant
Page 96 and 97:
Table 15. Effect of TCDD on the lev
Page 98 and 99:
Table 16c. Effcct of TCDD on the an
Page 100 and 101:
Table 18a. Effect of co-administrat
Page 103 and 104:
Table 21. Effect of co-administrati
Page 105 and 106:
Table 24b. Effect of co-administrat
Page 107 and 108:
Table 25c. Effect of co-administrat
Page 109 and 110:
Table 26d. Effect of co-administrat
Page 111 and 112:
Table 30. Effect of co-administrati
Page 113 and 114:
Table 32. Effect of caadrninistrati
Page 115 and 116:
Table 33c. Effcct of co-administrut
Page 117 and 118:
5 DISCUSSION 5.1 Significance of th
Page 119 and 120:
Measurement of weights of the acces
Page 121 and 122:
compartment of the cells (Chainy el
Page 123 and 124:
the reduction in daily sperm produc
Page 125 and 126:
eported in the TCDD-treated rats (M
Page 127 and 128:
lilnction is to ililcrccpt lipid pc
Page 129 and 130:
in the animals administered with TC
Page 131 and 132:
protective effects on serum testost
Page 133:
suygcstccl that vivamin 1: conld im
Page 136 and 137:
Fig.4~. ENect of TCDD or TCDD and v
Page 138:
tE W d In w it I I (,OCX) 3s PUB (,
Page 142 and 143:
Fig. 7c. Effect of TCDD or TCDD and
Page 145 and 146:
u 3 f ~ = m w * N O .- ~Slew aew en
Page 147 and 148:
Fig.lOb. ENmt of TCDD or TCDD and v
Page 151:
Fig. 1Ir Effect of TCDD or TCDD md
Page 158 and 159:
Fig. 14c. Effect of TCDD or TCDD an
Page 160 and 161:
Fig. 16b. Effect of TCDD or TCDD an
Page 164 and 165:
Fig.18~. EKect of TCDD or TCDD and
Page 166 and 167:
1 1.2 l4 Fig. 19b. ENect of TCDD or
Page 168 and 169:
Fig. ZOb. Elkt of TCDD or TCDD and
Page 171 and 172:
Fig. 21. Effect olTCDD or TCDD and
Page 173 and 174:
Fig. 22c. Effect of TCDD or TCDD an
Page 175 and 176:
Fig. 24b. Eflect ofTCDD or TCDD and
Page 177 and 178:
7 REFERENCES Aitken RJ, Irvine DS,
Page 179 and 180:
Chitm KC, Latchoumycandanc,C, Mathu
Page 181 and 182:
Flsher JS, Turner KJ, Brown D, Shar
Page 183 and 184:
Hornsby PJ. Regulation of cytochrom
Page 185 and 186:
Latcboumycandane C, Chitra KC, Math
Page 187 and 188:
Moore RW, Panona JA, Bookstaff RC,
Page 189 and 190:
Rommerts FFG, Cooke BA, Van Der Kem
Page 191 and 192:
Slaunwhite WR, Burgett MJ. h virro
Page 193 and 194:
1.1 Preparation of dosing solution
Page 195 and 196:
1.4.6 Wash concentrate One bottle,
Page 197 and 198:
1.7.3 Estradiol controls Two vials.
Page 199 and 200:
1.1 1.2 Orcinol(6%) 6 g of orcinol
Page 201 and 202:
1.16.2 Horseradish peroxidase (8 Un
Page 203 and 204:
1.20 Superoxide dismutase 1.20.1 Tr
Page 205 and 206:
1.24.2 Thiobarbituric acid (TBA; 0.
Page 207 and 208:
Chronic effect: of enclosulfan on t
Page 209:
enbw1h1.W mu IUY Wcab unpiliml~t at
Page 212 and 213:
cbniuis 11~11 b"nci:~lc ~wlive oxyg
Page 214 and 215:
DNA, RNA ;uxl Wcin wcrr abarval, wh
Page 216 and 217:
Mt~~m(10-lZsu&)vacob- Wfmn Ihehml ~
Page 218 and 219:
New Delhi, llrliil Ib SCI~KK Rcm& M
Page 220 and 221:
tiii~lc rcprmluction or rut (Cllitr
Page 222 and 223:
wciglit (b.wt.) per day for 45 days
Page 224 and 225:
0.1 00 01 " 0.8 I . .lo Dl* rcnn IW
Page 226 and 227:
Chilr:~. K.C.. L!olnn!myci!~dum. C.
Page 228 and 229:
C. hteboumyeradlos . KC. CMtn . P.P
Page 230 and 231:
I. 1 Ilal 01 2 1.7 # I c I ~ ~ L I
Page 232 and 233:
Fin. L Corrclatwn bclwfcn "perm cou
Page 235:
Iionshii nepmdvctivc mxicity ad upt
Page 240 and 241:
o. Glutathione reductage mg pmWn mg
Page 242 and 243:
IOWAME -. Tor. #558517 PME: 9 SESS:
Page 244 and 245:
JOBNAME: Rqm. Tm. M5W7 PAOB: 11 SBS
Page 246 and 247:
t 02 ELSEVIER Toricology OM) (2W1)
Page 248 and 249:
---- - wcre obtu~ncd from E-Monk. G
Page 250:
3.2. A,III~AILNI syrlo~t of ,nIroch
Page 253 and 254:
Uc,#!dy. SC. N;tdcru. S , 1% Conlrb
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