Reproductive changes in male rats treated perinatally with an aromatase inhibitor.

The effects of maternal exposure to aromatase inhibitor during the perinatal period of sexual brain differentiation were studied. The fertility was assessed in adult, male rat offspring of aromatase inhibitor-treated dams. The following results were obtained: (1) Sexual maturation, body weight, and wet weights of testis, pituitary, seminal vesicle, ventral prostate, and levatori ani muscle were unchanged at adult life. (2) Fifty percent of the animals were able to mate with normal females, which became pregnant but exhibited an increased number of preimplantation loss. (3) There was a decrease in the number of spermatozoa found in the testes and in the daily sperm production. (4) Of those, 25% of the male rats treated with aromatase inhibitor did not present male sexual behavior, showing female behavior when pretreated with estrogen. These results indicate that perinatal exposure to aromatase inhibitor during the critical period of male brain sexual differentiation has a long-term effect on the reproductive physiology and behavior of male rats

Effects of maternal exposure to an aromatase inhibitor on sexual behaviour and neurochemical and endocrine aspects of adult male rat

The present study examined the effects of letrozole exposure during brain sexual differentiation on endocrine, behavioural and neurochemical parameters in male rat descendants. Pregnant female rats received 1 mg kg(-1) day(-1) letrozole or vehicle by oral gavage on gestational Days 21 and 22. Exposure to letrozole reduced anogenital distance in males on postnatal Day (PND) 22. At adulthood (PND 75), plasma testosterone levels and hypothalamic dopaminergic activity were increased, but sexual competence was impaired, because fewer successful sexual behaviours (mount, intromission and principally ejaculation) were observed. The impairment of reproductive function by prenatal exposure to an aromatase inhibitor reinforces the importance of adequate oestrogenic activity during perinatal sexual differentiation for complete masculinisation of the hypothalamus

Semen parameters, fertility and testosterone levels in male rats exposed prenatally to betamethasone

The present study investigated the long-term effects of prenatal betamethasone exposure on sperm quality and count, fertility and plasma testosterone levels in adult male rats. Pregnant rats received 0.1 mg kg(-1) betamethasone on Days 12, 13, 18 and 19 of pregnancy. This treatment impaired sperm quality, sperm production, fertility and plasma testosterone levels in adult male offspring compared to the control group. Thus, the results of the present study indicate that the long-term effects of prenatal betamethasone exposure may be deleterious to offspring. The consequent decrease in testosterone production during adulthood, in association with damaged semen parameters, may explain for the observed decrease in the capacity of adult male offspring to themselves generate viable descendants.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Impairment of adult male reproductive function in rats exposed to ethanol since puberty

The objective of this work was to evaluate reproductive function in adult male rats exposed to ethanol since puberty. Male Wistar rats, 50 days old, received a liquid diet with 36% of the daily calories derived from ethanol or an isocaloric control diet for 55 days. The ethanol treatment impaired sexual behavior and only 22% of these rats reached ejaculation. The fertility of ethanol-treated animals was significantly reduced, mainly after natural mating. Serum testosterone levels, daily sperm production and sperm count in the epididymis were also significantly diminished after ethanol treatment, associated with an acceleration of the sperm transit time in the cauda epididymidis, decrease in sperm motility and increased percentage of abnormal shaped sperm cells. The results showed that chronic consumption of ethanol beginning at puberty impairs the reproductive function of adult male rats. (c) 2006 Elsevier B.V. All rights reserved

Ejaculatory Dysfunction In Streptozotocin-induced Diabetic Rats: The Role Of Testosterone.

Hyperglycemic and hypoinsulinemic states caused by diabetes mellitus are usually related to some type of sexual dysfunction, resulting in infertility in humans and experimental models, mostly due to their effects on ejaculatory function. This study aimed to evaluate the possible role of testosterone in the restoration of normal ejaculatory function in diabetic rats. Male Wistar rats were randomly allocated into 3 experimental groups: control, diabetic (streptozotocin), and diabetic with testosterone supplementation (streptozotocin plus testosterone). The following parameters were assessed at the end of the experiment: body weight, circulating testosterone levels, number of spermatozoa ejaculated in the uterus through natural mating, and weight and in vitro isometric contractions of the vas deferens. Diabetic rats showed reduced plasma testosterone levels and ejaculatory dysfunction as observed by a lack in the spermatozoa ejaculated into the uterus of receptive females. In these diabetic rats, no difference was observed in the sensitivity of the vas deferens to norepinephrine, with or without the presence of the cocktail (cocaine plus propranolol). In spite of this, an increased sensitivity to methoxamine through the α1-adrenoceptor was observed. Testosterone supplementation did not restore these parameters to control values.We conclude that, in this experimental model, the lack of testosterone was not directly related to the diabetes-induced ejaculatory dysfunction.63130-

Ejaculatory dysfunction in streptozotocin-induced diabetic rats: the role of testosterone

Hyperglycemic and hypoinsulinemic states caused by diabetes mellitus are usually related to some type of sexual dysfunction, resulting in infertility in humans and experimental models, mostly due to their effects on ejaculatory function. This study aimed to evaluate the possible role of testosterone in the restoration of normal ejaculatory function in diabetic rats. Male Wistar rats were randomly allocated into 3 experimental groups: control, diabetic (streptozotocin), and diabetic with testosterone supplementation (streptozotocin plus testosterone). The following parameters were assessed at the end of the experiment: body weight, circulating testosterone levels, number of spermatozoa ejaculated in the uterus through natural mating, and weight and in vitro isometric contractions of the vas deferens. Diabetic rats showed reduced plasma testosterone levels and ejaculatory dysfunction as observed by a lack in the spermatozoa ejaculated into the uterus of receptive females. In these diabetic rats, no difference was observed in the sensitivity of the vas deferens to norepinephrine, with or without the presence of the cocktail (cocaine plus propranolol). In spite of this, an increased sensitivity to methoxamine through the alpha(1)-adrenoceptor was observed. Testosterone supplementation did not restore these parameters to control values. We conclude that, in this experimental model, the lack of testosterone was not directly related to the diabetes-induced ejaculatory dysfunction.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Intrachromosomal amplification of chromosome 21 (iAMP21) detected by ETV6/RUNX1 FISH screening in childhood acute lymphoblastic leukemia: a case report

Chromosome abnormalities that usually define high-risk acute lymphoblastic leukemia are the t(9;22)/ breakpoint cluster region protein-Abelson murine leukemia viral oncogene homolog 1, hypodiploid with < 44 chromosomes and 11q23/ myeloid/lymphoid leukemia gene rearrangements. The spectrum of acute lymphoblastic leukemia genetic abnormalities is nevertheless rapidly expanding. Therefore, newly described chromosomal aberrations are likely to have an impact on clinical care in the near future. Recently, the rare intrachromosomal amplification of chromosome 21 started to be considered a high-risk chromosomal abnormality. It occurs in approximately 2-5% of pediatric patients with B-cell precursor acute lymphoblastic leukemia. This abnormality is associated with a poor outcome. Hence, an accurate detection of this abnormality is expected to become very important in the choice of appropriate therapy. In this work the clinical and molecular cytogenetic evaluation by fluorescence in situ hybridization of a child with B-cell precursor acute lymphoblastic leukemia presenting the rare intrachromosomal amplification of chromosome 21 is described