7 research outputs found
Development of germ cell neoplasia in situ in chinchilla rabbits
The present study was designed to describe
the development of germ cell neoplasia in situ in
Chinchilla rabbit by administration of estradiol. The
study was performed in rabbits distributed into two
groups: control and 17 β-estradiol. The determination of
histological alterations and POU5F1 and c-kit proteins
employed as biomarkers for the diagnosis of this
neoplasia was carried out. Testicular descent and
complete spermatogenesis were observed in the control
group. The protein biomarkers were negative. However,
in the rabbits treated with estradiol, the testes remained
undescended with the gonocytes undifferentiated to
spermatogonia. There were histological lesions owing to
germ cell neoplasia in situ and positive to POU5F1 and
c-kit proteins. These findings indicate that the chinchilla
rabbit is an ideal model to study this neoplasia in which
the histological characteristics and biomarkers of the
disease could be clearly observed. Using this model we
suggested that the persisting gonocytes could be
responsible for the development of germ cell neoplasia
in situ
Epigallocatechin-3-gallate protects the testis from damage generated by experimental cryptorchidism in rabbits
Cryptorchidism (CO) is a risk factor for
infertility in men. It is associated with an increase in
oxidative stress which alters the differentiation of the
gonocytes to spermatogonia. Epigallocatechin-3-gallate
(EGCG) is an antioxidant that acts as a free radical
scavenger and activates the antioxidant enzymes. The
aim of this work was to investigate if EGCG plays a role
in the protection of the testicle from alterations
generated by CO and its possible mechanism. Male
rabbits 7 days old were divided into four groups and
distributed as follows: 1) control (C) treated with EGCG
vehicle (V) (C/V); 2) C with administration of EGCG
from 65 to 120 days postpartum (dpp) (C/EGCG); 3) CO
induced by administration of 17β-estradiol plus EGCG
vehicle (CO/V) and 4) CO plus EGCG administration
(CO/EGCG). The animals were euthanized at 120 dpp
and their testes were processed to evaluate lipid
peroxidation, activities of superoxide dismutase (SOD)
and catalase (CAT) enzymes as well as serum
testosterone (T) concentrations. In addition, the rates of
apoptosis, cell proliferation and histological alterations
were determined. The CO/EGCG group showed a
significant reduction in lipid peroxidation, a significant
increase in the anti-oxidant enzyme activities and
concentrations of T. Also, there was a significant
decrease in the histological alterations, absence of
gonocytes and active spermatogenesis when compared
with CO/V group. These results show that EGCG
reduces lipid peroxidation and increases the activity of
the endogenous anti-oxidant system which protects the
testes from alterations produced by oxidative stress
generated during experimental CO
Fetal and Postnatal Nicotine Exposure Modifies Maturation of Gonocytes to Spermatogonia in Mice
Studies in laboratory animals have shown that male offspring from dams, exposed to nicotine during pregnancy and postnatal periods, show alterations in fertility, although the origin of this is still uncertain. In this study, we examined in a mouse model if the process of gonocyte maturation to spermatogonia was affected in male offspring from dams with nicotine administration during pregnancy and postnatal periods. BALB/C mice, with and without nicotine administrations in pregnancy and postnatal periods, were studied. The animals were euthanized at 3, 7, 10, 16, and 35 days postpartum (dpp). Testicular tissue samples were processed for histological, ultrastructural, and immunohistochemical studies; and testicular lipoperoxidation was determined. It was observed that in the nicotine-exposed animals, there was increased apoptosis and a reduction in the number of gonocytes that matured to spermatogonia. This gonocyte-spermatogonia maturation reduction was associated with a greater immunoreactivity to nicotinic acetylcholine receptors in the germ cells. Lipoperoxidation was similar in both groups until 16 dpp, with significant reduction at 35 dpp. Our findings suggest that nicotine intake during pregnancy and postnatal periods can affect the process of maturation of gonocytes to spermatogonia and the pool of available spermatogonia for spermatogenesis
Molecular Characterization of Patients with Cryptorchidism: Preliminary Search for an Expression Profile Related to That of Testicular Germ-Cell Tumors
Cryptorchidism (CO) is a risk factor for the development of testicular germ-cell tumors (TGCT). This is supported by reports showing the persistence of gonocytes in CO patients. These cells are proposed to be related to the development of germ-cell neoplasia in situ (GCNIS), which is considered the precursor stage/lesion of TGCT. Therefore, it is proposed that some patients with CO could express some molecular markers related to TGCT. In this study, we analyzed testicular tissue samples from CO, TGCT, and controls. We determined the expression of POU5F1, PLAP, and KIT by immunohistochemistry and that of the hsa-miR-371-373 cluster, hsa-miR-367, and LATS2, PTEN, and IGFR1 genes by RT-qPCR. We then carried out a bioinformatic analysis to identify other possible candidate genes as tumor biomarkers. We found that 16.7% (2/12) of the CO patients presented increased expression of POU5F1, KIT, PLAP, hsa-miR-371-373, and hsa-miR-367 and decreased expression of LATS2 and IGF1R. Finally, the genes ARID4B, GALNT3, and KPNA6 were identified as other possible candidate tumor biomarkers. This is the first report describing the expression of the hsa-miR-371-373 cluster, hsa-miR-367, LATS2, and IGF1R in the testicular tissues of two CO patients with cells immune-positive to POU5F1, PLAP, and KIT, which is similar to what is observed in TGCT