The dose dependent depletion of ovarian Ascorbic acid (AA) in rat ovaries, has been used as a bioassay for measurement of Luteinizing Hormone (LH). However, the mechanism of action of gonadotropin (LH, FSH) on ascorbic acid depletion is not completely clear in biochemical terms. To elucidate the mechanism, we looked for the pathways; one, where L-Gulonate Dehydrogenase (L-GuDH) catalyzes the conversion of L-Gulonic acid (L-GuA) to L-Xylulose, and, in the second the pathway conversion of L-GuA to AA, in a cats, dogs and Rats. Kinetic analysis of the enzyme L-GuDH in vitro showed the inhibitory effect of AA on L-GuDH. Therefore, we hypothesized that gonadotropins (FSH and LH) may regulate the L-GuDH maintain level of AA in ovary. LH administration to super-ovulated immature female rats caused depletion of ovarian AA but did not result in any change in the specific activity of the ovarian L-GuDH. Further, we administrated a surrogate FSH like hormone (PMSG) to immature female rats which, resulted in increased specific activity of ovarian L-GuDH. However, microarray data on RNA from ovaries exposed to FSH like hormone such as Pregnant Mare serum Gonadotropin (PMSG) did not reveal any increased expression of L-GuDH transcript. It is therefore concluded from the results obtained that; that neither LH, in decreasing the ovarian AA, nor FSH, in increasing the ovarian AA do so by regulating the activity of enzyme L-GuDH at transcriptional level. The results obtained have also been discussed by giving emphasis on the mechanism of ovarian ascorbic acid regulation of LH and FSH.

Regulation of Ascorbic acid by gonadotropins in rat Ovary