Efectos de exposición aguda a cadmio en la acción de estrógenos en útero de rata impúber / Effects of acute exposure to cadmiun on response to estrogen in the prepuberal rat uterus

Background: Few information is available about uterine effects of Cadmium (Cd) exposure, where toxic agents affecting the female genital tract interact with estrogen (E) receptors, modifiying myometrial activity and the menstrual cycle, causing dysmenorrhea, infertility and spontaneous abortion. No information exists whether prenatal or early postnatal exposure may cause any gynecologic persistent adverse effect. Our finding of a second mechanism of E interaction and differences between E receptors in the various uterine cell types suggests that Cd may affect differently E interaction in each cell-type. Objective: Evaluate a possible selective effect of acute Cd exposure on E action in the uterus during prepuber age. Method: Female prepuber rats exposed to Cd 4 mg/kg and 2 hours later, treated with Estradiol-17² 0,3 mg/kg. A myometrial sample was obtained under anaesthesia 24 hours after E treatment and histologically processed for the quantification of E responses on different uterine cell-types. Results: Cd exposure potentiates E-induced uterine eosinophilia and endometrial edema and inhibits E-induced cell hypertrophy in circular myometrium and cell proliferation in luminal myometrium. Cd, in the absence of hormone stimulation, causes a slight cell hypertrophy in circular myometrium. Conclusions: Acute exposure to Cd affects differently various responses to E in the different uterine cell-types. Future studies should verify whether this effect explains Cd-induced infertility, postpubertal sex organ development and whether prenatal or early postnatal exposure to Cd induces delayed persistent effects.

Antecedentes: Existe poca información sobre efectos del cadmio (Cd) en el útero. En mujeres altera la actividad miometrial, el ciclo menstrual y causa dismenorrea, abortos espontáneos, infertilidad y mortinatos. No existe información si la exposición prenatal o postnatal temprana causa efectos ginecológicos diferidos persistentes. Los tóxicos que afectan el útero suelen interactuar con receptores de estrógeno (E). Nuestro hallazgo de un segundo mecanismo de acción de E y de diferencias entre receptores de E de los diversos tipos celulares uterinos hacen posible que el Cd interactúe con los E en forma diferente en cada tipo celular. Objetivos: Buscar un posible efecto selectivo de la exposición aguda a Cd con algunas respuestas a E en útero de rata durante la edad prepuberal. Métodos: Ratas hembra impúberes recibieron 4 mg Cd/kg p.c. y 2 h después se trataron con 0,3 mg estradiol-17(3/kg p.c; los úteros fueron obtenidos bajo anestesia a las 24 h del tratamiento con E. Los úteros se procesaron para la cuantificación de respuestas a E en cada tipo celular por separado. Resultados: La exposición a Cd incrementa la eosinofilia uterina y edema endometrial inducidos por E; inhibe las siguientes respuestas a E: hipertrofia celular en miometrio circular, proliferación celular en epitelio luminal y miometrio. En ausencia de hormona, el cadmio causa una leve hipertrofia celular en miometrio circular. Conclusiones: La exposición aguda a Cd afecta de manera diferente las respuestas a E en los diversos tipos celulares uterinos de rata prepuberal. Futuros estudios deberán verificar si este efecto explica la infertilidad causada por exposición a Cd, afecta el desarrollo postpuberal de los órganos sexuales, e investigar si la exposición prenatal o postnatal temprana induce efectos diferidos persistentes, como puede ocurrir en población infantil prenatalmente expuesta a Cd.

Effect of chronic exposure to lead on estrogen action in the prepubertal rat uterus.

Lead is a widely spread environmental pollutant known to affect both male and female reproductive systems in humans and in experimental animals. The present study investigated the effect of a chronic exposure to lead on different parameters of estrogen stimulation in the uteri of prepubertal rats. Chronic exposure to lead enhanced some parameters of estrogen stimulation, inhibited other estrogenic responses, while the remainder were unaltered. Estrogen-induced uterine eosinophilia (24 h), the proportion of uterine eosinophils in the mesometrium (6 h), and luminal epithelial hypertrophy and RNA content (24 h) appeared to be enhanced by lead exposure, compared to lead-unexposed control animals. Eosinophilia in the endometrium (6 h), the proportion of uterine eosinophils in the endometrium (6 and 24 h), edema in superficial and deep endometria (6 h), luminal epithelial hypertrophy (6 h), and mitotic response (cell proliferation) in all uterine cell types were inhibited by lead exposure, whereas circular myometrial hypertrophy was not significantly modified. The effects of lead exposure on responses to estrogen found in this study showed some differences with those previously reported for acute or subacute exposure to lead. The results revealed an interaction with the different mechanisms of estrogen action in the uterus at various levels, suggesting that some uterine cell types are more sensitive to lead than others. The relevance of the results for lead-induced infertility is discussed in this article, and possible mechanisms of action are proposed.

Studies on parasitemia courses and mortality in mice infected with genetically distant Trypanosoma cruzi clonets

The biological characterization of bloodstream forms of eleven Trypanosoma cruzi cloned stocks, corresponding to two genetically similar clonets (19 and 20) and one distant clonet (39), according to multilocus enzyme electrophoresis analysis, showed dissimilar parasitemia in an experimental isogenic mouse model. While clonet 39 stocks gave low parasitemias, clonets 19 or 20 stocks gave high parasitemias, independently of the inocula (102 and 104 bloodstream forms) used. High parasitemia did not always associate with greater mortality. Statistical studies on mortality using a low inocula showed significantly higher mortality with clonet 39 stocks when compared to clonets 19 or 20 stocks. Finally, in order to confirm the identity of each stock studied, typing by molecular karyotype was performed before inoculating mice.