[Changes in pancreatic arginase activity in pubertal and adult rats induced by castration]. / Cambios en la actividad de arginasa pancreática en ratas púberes y adultas inducidos por la castración.

Arginase activity in kidney, and small intestine in several mammalian species is sensitive to castration, a finding that could suggest their dependence on testosterone. However, as far as we know, information on regulation of pancreatic arginase activity is scarce. In this paper, the effect of orchidectomy on pancreatic arginase activity in pubescent and adult rats was studied. Male pubescent and adult rats, 21 days old and 4 months old, respectively, were orquidectomizades and sacrificed at various times post-surgery. Groups of intact rats served as controls. Arginase activity and proteins were measured in pancreatic tissue. The activity of this enzyme was measured in serum in addition to glucose, triglycerides and total proteins. In pubescent rats pancreatic and serum arginase activities peaked at day 5 post-surgery, increased arginase activity in adult rats was seen at day 20. Changes in serum and pancreatic proteins in pubescent, but not in adult, castrated rats were observed. Taken together, these results suggest that pancreatic arginase activity is androgen-dependent and that there is age-difference, probably due lo distinct patterns of hormone secretion in pubescent and adult rats.

Prevention by L-arginine and polyamines of delayed development and embryotoxicity caused by chemically-induced diabetes in rats.

Diabetes mellitus induction with alloxan at a dose of 110 mg/kg i.p. in rats on Day 4 of pregnancy causes delayed development and resorptions as signs of embryotoxicity. In the present study, the administration of human NPH insulin at doses of 1 to 5 U/d to rats or 1.0 mL of 10 mM L-arginine for 8 d, starting the day following diabetes induction, prevented embryotoxicity and delayed development. Similar results were obtained when the polyamines putrescine, spermidine, or spermine were administered at doses of 1.0 mL of a 10 microM solution to each rat daily. However, even though L-arginine and polyamines prevented adverse effects of severe diabetes on the conceptus, and caused normalization of glucose, beta-hydroxybutyrate levels remained elevated. These results support the hypothesis that the mechanisms of normal and altered development could be mediated by the action of polyamines.

[Hypoglycemia as a risk factor in embryonic development in maternal diabetes mellitus. Review of the literature]. / La hipoglucemia como factor de riesgo sobre el desarrollo embrionario en diabetes mellitus. Revisión bibliográfica.

Hypoglucemia, or decrease in normal blood glucose concentration, is an important sequel of tight control of type 1 diabetic patients. In pregnant diabetic women, hypoclycemia does not appears affect the embryo or fetal development; while in rodent, it is an important cause of teratogenesis and/or embryotoxicity, when it is presented during organogenesis. Despite metabolic, endocrine and temporal differences between human and rodent pregnancy, a possible damage to the product, caused by hypoblycemia during pregnancy in human, must be considered.

Fetal development in alloxan-treated rats.

The effect of alloxan on embryo and fetal development in rats was evaluated. Alloxan was injected intraperitoneally (ip) in pregnant rats at doses of 80 to 150 mg/kg at Day 0 (day of fertilization), and 110 mg/kg at Day 4 of pregnancy. Hyperglycemia was rarely produced at alloxan doses from 80 to 100 mg/kg, and the frequency of malformations observed was low. Higher doses (110 to 150 mg/kg) caused severe hyperglycemia, and maternal or embryonic death. When 110 mg/kg was administered on Day 4 of gestation (the day before embryo implantation), all rats had resorption nodules and litters with embryos with delayed growth. We recommend the induction of diabetes mellitus on Day 4 of pregnancy for studies of diabetes-gestation interaction.

[Molecular systems in cellular interactions. I. Fertilization iin mammals]. / Sistemas moleculares en las interacciones celulares. I: Fecundación en mamíferos.

Multicellular organisms require diverse mechanisms of cellular recognition in order to work integrally. In the present paper we consider the molecular mechanisms for cell recognition and cell adhesion on fertilization of mammalian egg. Several surface proteins of spermatozoa (galactosyl transferase, proteases, glycosidases and lectins), recognize and bind zona pellucida glycoproteins of egg, a necessary condition prior to fertilization.

[Mechanism of action of steroid hormones. I. Estrogens]. / Mecanismo de acción de hormonas esteroides. I. Estrógenos.

The steroid hormone are very versatile molecules: although they are related among them by their chemical structure, they have very diverse functions and including antagonic. Their action mechanism is not completely cleared. The estrogens participate in the regulation of practically all the reproductive and sexual events of the female, although the intracellular actions by which they take place are not well known and the proposed models do not adequately satisfy the questions. Currently it is accepted the existence of a cytoplasmic and/or nuclear receptor, without explaining satisfactorily how the hormones come to the nucleus. The endocrine events that are rapidly expressed (seconds) are due to a possible interaction with cellular membrane. The purpose of this review is to analyze and concilliate the reported data on the mechanism of action of estrogens.

[Uterine contraction. Mechanism, regulation and pharmacology]. / Contracción uterina. Mecanismo, regulación y farmacología.

Uterine contraction is essential for genital tract functioning among mammal females. For women, the main interest are the possible alterations, and the ability to manage them with drug use. Due to the fact that contraction regulation is multifactorial, several medications are used in basic and clinical research, both to know contraction mechanisms, and to interfere with its alterations. This review considers contraction mechanism at molecular-cellular level, and the different molecules regulating it; as well as the effects that different medications produce upon such mechanism.