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PubMed1982

Factors affecting testis weight in normal and cryptorchid horses.

Testes were collected from normal and cryptorchid horses of a variety of breeds and ages and weighed after dissection from the epididymis. Scrotal testes grow little until the second winter of life and little thereafter, although a nearly mature body weight is reached by the end of the first winter. Scrotal testes in unilateral cryptorchids tend to be larger than those of normal stallions, sometimes exceedingly so, although occasional small scrotal testes are recorded. Inguinal testes show some tendency to grow during the second winter but the data are difficult to analyse beyond that age because of the transient nature of most cases of inguinal cryptorchidism. Abdominal testes do not appear to increase in size with age but if a unilateral abdominal cryptorchid has its scrotal testis removed, the remaining abdominally retained testis undergoes marked hypertrophy.

Aging↗
PubMedDate not supplied

Correlated responses in male reproductive traits in mice selected for litter size and body weight.

Correlated responses in male reproductive traits were determined at 4, 6 and 8 weeks of age in lines of mice selected for large litter size (L+), large 6-week body weight (W+), large litter size and small body weight (L+W-) and small litter size and large body weight (L-W+), and in an unselected control (K). Concentration of serum testosterone and weights of testes, seminal vesicles, epididymides and adrenal glands increased with age. Line differences in testosterone concentration were not detected. L+ and W+ males exhibited positive correlated responses in testes, epididymides and seminal vesicle weights. Testis weight adjusted for body weight was significantly larger for L+ than controls and approached significance for W+. Realized genetic correlation be-testis weight and litter size was 0.60 +/- 0.04, and the realized partial genetic correlation holding body weight constant was 0.42. Therefore, pleiotropic loci, acting via the hypothalamic-pituitary axis, affect testis weight and litter size independently of body weight. Additionally, genes influencing overall growth have a pleiotropic effect on testis weight and litter size in mice; the realized genetic correlations of body weight with testis weight and with litter size were 0.60 +/- 0.03 and 0.52 +/- 0.10. Testis weight increased in both L+W- and L-W+ males. The positive correlated response in L+W- may have resulted from changes in frequency of genes controlling reproductive processes; whereas, in L-W+ it could have been the result of changes in the frequency of genes associated with body weight.

Adrenal Glands↗
PubMed1998

Centromere protein B null mice are mitotically and meiotically normal but have lower body and testis weights.

CENP-B is a constitutive centromere DNA-binding protein that is conserved in a number of mammalian species and in yeast. Despite this conservation, earlier cytological and indirect experimental studies have provided conflicting evidence concerning the role of this protein in mitosis. The requirement of this protein in meiosis has also not previously been described. To resolve these uncertainties, we used targeted disruption of the Cenpb gene in mouse to study the functional significance of this protein in mitosis and meiosis. Male and female Cenpb null mice have normal body weights at birth and at weaning, but these subsequently lag behind those of the heterozygous and wild-type animals. The weight and sperm content of the testes of Cenpb null mice are also significantly decreased. Otherwise, the animals appear developmentally and reproductively normal. Cytogenetic fluorescence-activated cell sorting and histological analyses of somatic and germline tissues revealed no abnormality. These results indicate that Cenpb is not essential for mitosis or meiosis, although the observed weight reduction raises the possibility that Cenpb deficiency may subtly affect some aspects of centromere assembly and function, and result in reduced rate of cell cycle progression, efficiency of microtubule capture, and/or chromosome movement. A model for a functional redundancy of this protein is presented.

Animals↗
PubMed1995

Clastogenic effects of 1,3-butadiene and its metabolites 1,2-epoxybutene and 1,2,3,4-diepoxybutane in splenocytes and germ cells of rats and mice in vivo.

Clastogenicity of 1,3-butadiene (BD), 1,2-epoxybutene (EB), and 1,2,3,4-diepoxybutane (DEB) was studied in splenocytes and germ cells of rats and mice by means of micronucleus assays (cytokinesis-block method for splenocytes, suspension method for germ cells). Inhalation exposure of mice to 200, 500, or 1,300 ppm BD (6 h/d; 5 days) induced significant chromosome damage in spermatocytes at the preleptotene stage. EB and DEB induced significant amounts of clastogenic damage in splenocytes and spermatocytes of rats and mice. The lowest tested effective doses for mice and rats were, respectively, 40 and 80 mg/kg for EB, and 15 and 30 mg/kg for DEB. In splenocytes, 80 mg EB/kg induced 3.6 times more MN in mice than in rats, whereas 30 mg DEB/kg induced the same amount of damage in both species. Damage in germ cells of mice was induced in early spermatocytes treated with 40 and 80 mg EB/kg, and in late spermatocytes exposed to 30 mg DEB/kg. In rats, 40 mg EB/kg induced damage in early spermatocytes, whereas 80 mg EB/kg induced chromosomal damage in early and late spermatocytes. In rats treated with DEB, clastogenic damage was induced in spermatocytes at preleptotene, zygotene, diplotene, and diakinesis stages. When the clastogenic potential of EB and DEB in splenocytes and germ cells of mice and rats was compared, DEB always showed a stronger effect than EB. Body weight, testis weight, ratio of testis weight to body weight, and ratio of Golgi to Golgi + cap phase spermatids were used as parameters for toxicity. Exposures to 500 and 1,300 ppm BD were somewhat toxic to mice. Doses of 80 mg EB/kg and 30 mg DEB/kg exhibited toxic effects in mice and rats.

Administration, Inhalation↗
PubMed1998

Pattern of messenger ribonucleic acid expression of tissue inhibitors of metalloproteinases (TIMPs) during testicular maturation in male mice lacking a functional TIMP-1 gene.

It has been proposed that proteolytic remodeling of the testicular extracellular matrix (ECM) plays a fundamental role in testicular development, morphogenesis, and spermatogenesis. Tissue inhibitor of metalloproteinase (TIMP)-1 regulates ECM turnover and has been reported to stimulate Leydig cell steroidogenesis. To assess the developmental changes in TIMP mRNA expression and the potential steroidogenic role of TIMP-1 in testicular physiology, an experiment was conducted that used male mice incapable of expressing the TIMP-1 gene product. TIMP-1-deficient and wild-type male mice (n = 6 to 15 per age group per genotype) were killed at 18, 21, 24, 27, 33, 41, and 49 days of age. Body weight, testis weight, serum total testosterone, and TIMP-1, -2, -3, and -4 transcript expression were determined. Northern analysis revealed the detection of TIMP-1 mRNA in wild-type males only. TIMP-1 mRNA levels (per 20 microg total RNA) were highest in 18- to 27-day-old male mice and decreased approximately 13-fold by Day 41. The pattern of TIMP-2 expression was similar between genotypes, with testicular levels of the 1. 0-kilobase transcript increasing between Days 18 and 27 of age. The pattern of TIMP-3 transcript expression (per 20 microg total RNA) was similar between genotypes and decreased between Days 18 and 41 of age. When TIMP-3 mRNA levels were expressed on a per testis basis, TIMP-3 was seen to have increased throughout testicular development. TIMP-4 mRNA expression was undetectable by Northern analysis in all mice. No significant difference was detected in body weight or testis weight between genotypes, with the exceptions that 21-day-old TIMP-1 mutants had higher (p < 0.05) testis weights and lower (p < 0. 05) serum total testosterone levels than age-matched wild-type males. It is concluded that each TIMP displays its own unique pattern of expression during the prepubertal period, suggesting that the various TIMPs may have specific roles in testicular development. The modest effect of TIMP-1 ablation on testosterone is interpreted to mean that TIMP-1 may function as a coregulator of basal testicular steroidogenesis; but overall, TIMP-1 appears to have little effect on testosterone production in mice lacking the TIMP-1 gene.

Aging↗
PubMed2004

Effects of Vitamin C and E on PCB (Aroclor 1254) induced oxidative stress, androgen binding protein and lactate in rat Sertoli cells.

The effect of Aroclor 1254 and the ameliorative effect of Vitamin C and E on Sertoli cell function were studied in adult male rats. The rats were administered Aroclor 1254 at a dose of 2 mg/kg bw/day intraperitoneally for 30 days. One group of rats received Vitamin C (100 mg/kg bw/day) while the other group received Vitamin E (50 mg/kg bw/day) orally simultaneously with Aroclor 1254 for 30 days. Necropsy was performed at 24 h after the last injection. Sertoli cells were isolated for the estimation of enzymatic antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GST), and gamma-glutamyl transpeptidase (gamma-GT). Lipid peroxidation (LPO), hydrogen peroxide and hydroxyl radical were estimated. Sertoli cellular androgen binding protein (ABP) and lactate were also quantified. Whereas body weight, testis weight, relative weight of testis, ABP, lactate and specific activities of SOD, CAT, GPx, GR, GST, gamma-GT were all decreased, the levels of hydrogen peroxide, hydroxyl radical and LPO were significantly increased in the Sertoli cells of Aroclor 1254 treated rats. Simultaneous administration of Vitamin C or E restored these parameters to a normal range. Thus, the present study suggests that Aroclor 1254 exposure induces oxidative stress in rat Sertoli cells and furthermore that simultaneous administration of Vitamin C or E ameliorated these effects.

Androgen-Binding Protein↗
PubMedDate not supplied

Sexual maturation in underfed weight-matched rats. A test of the "critical body weight" theory of pubertal timing in males.

A popular current theory proposes that the timing of puberty is related to attainment of a critical level of body weight or body fatness. These critical body weight and critical body fat theories have been studied almost exclusively in females. To explore these theories in males, we tested a corollary of these hypotheses: are male rats of the same weight all at the same level of sexual maturation irrespective of prior growth rate? Male rats growing in body weight at five different rates due to various degrees of underfeeding (beginning at weaning) were sacrificed at body weight milestones of 123 and 279 grams. At the first weight milestone, significant (P less than 0.01) inverse correlations were observed among these weight-matched rats between the preceding rate of body weight growth and prostate weight, seminal vesicle weight, testis weight, serum testosterone, and daily sperm production rate, indicating that the underfed animals were more sexually mature. Testis histology also showed that spermatogenic development increased progressively as the prior rate of body weight growth was reduced. These parameters of sexual maturation tended to correlate inversely with body fatness (i.e., leaner animals were more sexually mature) and directly with body length (i.e., longer animals were more sexually mature). By the second body weight milestone, however, the degree of prior underfeeding exerted little effect on those indices of sexual development. We conclude that the degree of sexual maturation in weight-matched animals with varying previous patterns of body weight growth correlates inversely with body fatness and the rate of body weight growth but correlates directly with body length.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMedDate not supplied

Testicular activity in mice selected for increased body weight.

Parameters of testicular function were studied in mice selected for increased body weight and in contemporaneous unselected controls. Spermatogenesis occurred at the same time in the two lines. Body weight, testis weight, mean seminiferous tubular diameter and serum testosterone were increased significantly in the high growth mice. It is suggested that some genetically determined differences in body size are brought about by the differential secretion of testosterone.

Age Factors↗
PubMed1977

Effect of long-term hyperbaric He-O2 exposure on the weight and histology of endocrine organs in growing rats.

The effects of long-term hyperbaric exposure on endocrine organ weight and histology and on epiphyseal-plate width were studied in growing male rats. Six groups of rats were exposed to 21 ATA He-O2 (200 mmHg O2), and six groups were maintained at 1 ATA as room-air controls. Each group contained eight rats. At intervals of of 2, 3, 5, 8, 10, and 12 weeks, one group was decompressed and studied along with a paired control group. Results indicated no changes in pituitary and adrenal gland weights. Testis weights were variable but histology and sperm content were normal. Only the accessory sex organs decreased significantly in weight; however, prostate and seminal vesicle histology were normal. Tibial epiphyseal-plate width was reduced in 21-ATA groups. These results suggest that long-term hyperbaric exposure has little effect on endocrine organs of the rat and observed weight changes are probably related to the reduced body weights.

Adrenal Glands↗
PubMed1999

Short term pretreatment with medroxyprogesterone and testosterone may potentiate irradiation damage to spermatogenesis in rats.

BACKGROUND: Hormonal treatments lasting 2-6 months inhibit spermatogenesis in men and have been proposed as germ cell protection against anticancer therapy. Because it is unthinkable to delay anticancer treatments, the authors investigated the protection afforded against irradiation of rats by 22 days of hormonal pretreatment. METHODS: Adult Sprague-Dawley rats were assigned to an untreated control group (C) or to one of 5 treatments: medroxyprogesterone acetate plus testosterone only (M), 3 or 5 gray of irradiation (R3 and R5), or hormonal treatment prior to 3 or 5 gray of irradiation (MR3 and MR5). Mating trials were conducted 1, 24, 45, 65, 86, and 109 days after treatment. At 122 days, genital organ weights, testis histology, and epididymal spermatozoa were evaluated. RESULTS: Irradiation reduced sperm production and had a clastogenic effect on postmeiotic germ cells. No protective effect of steroid treatment was observed. Moreover, testis weight, tubule diameter, the repopulating index, and the sperm head count decreased more in the MR5 group than in the R5 group. Mating tests showed decreases in positive vaginal smears and fertility at both 45 and 65 days, and an increase in resorption at 109 days. CONCLUSIONS: These results indicate that hormonal pretreatment potentiates irradiation damage to germ cells, especially stem cells, as regards survival and genomic alterations, probably because of increased lipoperoxidation of late spermatids.

Animals↗