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

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1997). This deficiency is characterized in adult rats by decreased plasma testostcronc<br />

and DHT concentrations, unaltered plasma LH concentrations and unchanged plasn~a<br />

clearance of androgens and LH (Moore er al., 1985; Moore el ul., 1989). The doserelated<br />

reduction in plasma testosterone and DHT concentrations along with the<br />

weights of the seminal vesicles and ventral prostate weights in rats has been reported<br />

(Moore er a/., 1985). In contrast, TCDD did not affect accessory sex organ weights in<br />

castrated adult rats implanted with either testosterone or DHT containing capsules<br />

(Bookstaff er al., 1990). Trophic responsiveness of the seminal vesicles and ventral<br />

prostate to testosterone and DHT has been shown to remain unaffected by<br />

postpubertal TCDD treatment TCDD could increase responsiveness of the pituitary to<br />

these androgens without affecting the responsiveness of the accessory sex organs<br />

(Gray er al., 1997). TCDD has been shown to increase epididyrnal transit rate of<br />

sperm through the cauda epididymis of rat primarily due to decreased transit rate ol'<br />

sperm through the caput and corpus epididymis (Wilker er al., 1996).<br />

1.3.1.3 Mechanism of TCDD action<br />

TCDD has been shown to act through aryl hydrocarbon receptor (AhR).<br />

AhR has been shown to modulate the expression of a number of phase I and phase I1<br />

enzymes responsible for detoxification1 bioactivation of a variety of lipophilic<br />

compounds (Hankinson, 1995). This modulation has been shown to be accomplished<br />

through ligand AhR complex interactions with specific DNA response elements called<br />

dioxin-response elements or xenobiotic-response elements (Safe, 1995). A number of<br />

genes, which are involved in the oxidative metabolism, havc been shown to be<br />

induced by the AhR including CYPIA1, CYPl A2 and CYPl Bl (Spink el 01.. 1990;<br />

Spink ef al., 1994; Safe. 1995; Hankinson. 1995). TCDD has been shown to induce<br />

the production of reactive oxygen species thereby causing oxidative stress in multiple<br />

tissucs through AhR activation or AhR mediated xanthine oxidascl santhinc<br />

dehydrogenase activity (Stohs, 1990: Safe, 2001; Sugihara o 01.. 2001). Thc<br />

mechanism of TCDD mediated reactive oxygen species production has been proposed<br />

to involve cytochrome P450s (Park el ol., 1996;.

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