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

een reported that TCDD decreases volume of the smooth e~idoplasmic reticulum and
mitochondria per testis and has been shown to alter testicular steroidogenesis in rats
and thereby reduce the production of testosterone and estradiol in rats (Wilker, 1996).
The decrease in the serum testosterone levels in adult rats could be due to the
diminished responsiveness of Leydig cells to LH and or the direct inhibition of
testicular steroidogenesis. It has been reported that two of the steroidogenic enzymes
involved in the conversion of cholesterol to testosterone in Leydig cells are
cytochrome P450 enzymes (P450scc and P450c17). Molecular oxygen and electrons
donated from NADPH were used for hydroxylation of the substrate. During normal
steroidogenesis, ROS (superoxide anion and or hydroxy radical) can be produced by
electron leakage outside the electron transfer chains (Homsby and Crivello, 1983;
Hanukoglu el al., 1993), and these free radicals can initiate lipid peroxidation, which
can inactivate P450 enzymes (Homsby, 1980). The inability of the pseudosubsuate to
be oxygenated promotes the release of reactive oxygen species (Peltola et al., 1996).
It has been reported that increased production of reactive oxygen species following
lindane treatment decreased the activities of steroidogenic enzymes in testis of rats
(Sujatha el a/.. 2001).
The levels of serum FSH and LH remained unchanged while the level of
prolactin decreased significantly in the animals administered with TCDD (Fig. 7c to
7e; Table 4). This is supported by previous reports that TCDD does not alter serum
FSH and LH levels in rats (Moore er 01..
1989) thereby suggesting that pituitary
hypofunction may not be a major cause of the initial stages of subchronic TCDD
toxicity. It has also been suggested that growth retardation in TCDD-treated rats may
not be the result of a deficiency of growth hormone (GH), alterations in plasma
conicosterone concentrations may due to altered responsiveness of the adrenal to
ACTH stimulation rather than to changes in plasma ACTH concentrations. and that
impaired spermatogenesis may not be associated with a decrease in plasma FSH
concentrations (Moore el ul., 1989).
l'hc levels of scruni prolnctili dccrcucd
significantly in the animals wated with TCDD. Similar changes have also been