Role of zinc in regulating the testicular function. Part 2. Effect of dietary zinc deficiency on gonadotropins, prolactin and testosterone levels as well as 3β-hydroxysteroid dehydrogenase activity in testes of male albino rats
SUMMARY
Administration of 100 μg prolactin twice daily for 3 days increased 3β-hydroxysteroid dehydrogenase (3β-HSD) activity in the testes of dwarf mice compared with that found in the normal mouse. In hypophysectomized rats, prolactin (200 μg, same regimen) was without effect when given alone, whereas 5 μg luteinizing hormone (LH) alone injected twice daily, increased 3β-HSD activity to above normal. When prolactin and LH were administered in combination, 3β-HSD activity was raised to normal levels only.
In Reply.—
We thank Nishi et al for outlining the role that has been suggested for zinc in normal testicular function and the speculation that zinc deficiency might contribute to the hypergonadotropic hypogonadism found in males with chronic renal failure. We have no data concerning zinc levels in our patients, and so we felt we could offer no further insight into the possibility that zinc deficiency might play a role in the etiology of the hypergonadotropism we described.
1. Pregnant rats were fed either low (less than 1 p.p.m.) Zn or control (40 p.p.m. Zn) diets from day 10 of gestation. They were killed at intervals during the last 96 h preceding the normal time for onset of parturition, and differences in plasma progesterone, oestradiol-17 beta and ovarian 20 alpha-hydroxysteroid dehydrogenase were assessed. 2. Gestation was prolonged in Zn-deficient rats. 3. Although the preparturient decline in plasma progesterone began at the same time in all groups, at term, plasma progesterone concentration in Zn-deficient rats remained significantly higher than in normal females. 4. Induction of ovarian 20 alpha-hydroxysteroid dehydrogenase activity was delayed by about 8 h by Zn deficiency. This delay was not observed if prostaglandin F2 alpha was injected previously. 5. The results suggest a Zn-dependent step(s) in uterine synthesis and/or release of prostanoids.
Lysophosphatidic acid (LPA) modulates prostaglandin (PG) synthesis via LPA receptor 3 (LPAR3) in the murine endometrium. The lack of functional LPAR3 in mice may lead to embryo mortality. In the present study, we examined the role of LPA in the bovine uterus. We confirmed that LPA is locally produced and released from the bovine endometrium. Moreover, there are enzymes involved in LPA synthesis (phospholipase(PL)D2and PLA2G1B) in the bovine endometrium during estrous cycle and early pregnancy. Expression of the receptor for LPA (LPAR1) was positively correlated with the expression ofPGE2synthase(PGES) and negatively correlated with the expression ofPGF2αsynthase(aldose reductase with 20 α-hydroxysteroid dehydrogenase activity –PGFS) during early pregnancy.In vivoLPA induced P4 and PGE2secretion was inhibited by LPAR1 antagonist (Ki16425). The overall results indicate that LPA is locally produced and released from the bovine endometrium. Moreover,LPAR1gene expression in the endometrium during the estrous cycle and early pregnancy indicates that LPA may play autocrine and/or paracrine roles in the bovine uterus.LPAR1gene expression is positively correlated with the expression of the enzyme responsible for luteotropic PGE2production (PGES) in endometrium. In cow, LPA stimulates P4 and PGE2secretion. Thus, LPA in the bovine reproductive tract may indirectly (via endometrium) or directly support corpus luteum action via the increase of P4 synthesis and the increase of PGE2/PGF2αratio. It suggests that LPA may serve as an important factor in the maintenance of early pregnancy in cow.
MORPHOMETRIC AND HISTOPATHOLOGICAL CHANGES INDUCED BY MODERATE AND SEVERE DIETARY ZINC DEFICIENCY IN TESTES OF MALE ALBINO RATS