Impact of Gestational and Lactational Exposure to Hexavalent Chromium on Steroidogenic Compartment of Post-Natal Rat Testis

Reproductive and embryonic toxicity of hexavalent chromium (CrVI) is known, and adult testis is one of its vulnerable targets. However, it is not known if gestational and lactational exposure to excess Cr affects development and functions of Leydig cells during postnatal life. It is hypothesized that gestational/lactational exposure to CrVI may affect Leydig cell development and differentiation and its functions during postnatal life extending into adulthood. Pregnant [gestational days 9 to 21] and lactating [postnatal days (PND) 1 to 21] rats were exposed to 50ppm and 100ppm CrVI (K₂Cr₂O₇) through drinking water, and testis was collected on PND 30, 60, 90 and 120, and subjected to light and transmission electron microscopic analysis. Serum testosterone and estradiol were determined adopting RIA. Histological evaluation of testes revealed hypertrophy and vacuolation of Leydig cells of CrVI-exposed rats; transmission electron micrographs (TEM) showed lipid accumulation, swollen mitochondria and disorganized smooth endoplasmic reticulum. Lactational exposure to CrVI led to decrease in the number of mitochondria and collapse of mitochondrial cristae. In general, the changes were obvious in PND 30 rats, and became less pronounced by PND 60 to become normal by PND 90. Serum testosterone and estradiol levels showed a general trend of opposite response to CrVI exposure. Gestational exposure to CrVI caused increase in testosterone level in prepuberal rats, but the trend was reversed by PND 60, and by PND 120 its level was more than in coeval controls. A similar trend was noticed in rats which had lactational exposure to CrVI but for a consistent increase in both steroids in PND 30 and PND 60 old rats which were exposed to 50ppm CrVI. By PND 90, testosterone remained elevated or normal, but by PND 120 its level was increased due to lactational exposure to CrVI. On the contrary, serum estradiol in these rats was low by PND 90 and became normal by PND 120. The findings partially support the hypothesis proposed and it is concluded that the fetal type Leydig cells are the major targets for the toxic effects of CrVI exposure during gestational and lactational periods where in lactational exposure may have a persistent effect leading to increased testosterone: estradiol ratio. Nevertheless, the effects of CrVI on testosterone and estradiol are reversible, as the adult type Leydig cells are unaffected.